Pub Date : 2022-09-01DOI: 10.12047/j.cjap.6269.2022.090
Ying-Xia Yang, Yu-Fen Guo, Hong-Hong Huang, Ling-Xing Wang
Objective: To investigate the effects of Butylphthalide on the expressions of HMGB1 and RAGE in frontal lobe of rats after chronic sleep deprivation.
Methods: Chronic sleep deprivation and butylphthalide treatment was performed in Sprague Dawley(SD)rats and the rats were divided into three groups (n=6): platform control group, chronic sleep deprivation group and chronic sleep deprivation + butylphthalide intervention group. Rats suffering chronic sleep deprivation were put in multiple platforms box for 18 h per day and sleep deprivation lasted for 28 days. Rats in butylphthalide intervention group were intraperitoneally injected with butylphthalide 100 mg/(kg·d) for 14 days after sleep deprivation. After collecting brains, high-mobility group box (HMGB1) and nuclear transcription factor kappB (NF-κB)p65 were detected by immunohistochemistry. The expression of HMGB1, silent information regulator of transcription 1 (SIRT1), receptor for advanced glycation end-products (RAGE) and NF-κB in frontal lobe were determinated by Western blot.
Results: Compared with platform control group, the expression levels of HMGB1, RAGE and nuclear NF-κB p65 were increased significantly, while the expression of SIRT1 was decreased siginificantly in frontal lobe of chronic sleep deprivation group (all P<0.05). Compared with chronic sleep deprivation group, the expression levels of of HMGB1, RAGE and nuclear NF-κB p65 were decreased significantly, while the expression of SIRT1 was increased significantly in chronic sleep deprivation + butylphthalide intervention group (all P<0.05).
Conclusion: Butylphthalide can inhibit HMGB1/RAGE/NF-κB pathway in frontal lobe of rats after chronic sleep deprivation by changing the expression of HMGB1 and RAGE, and reducing the nuclear translocation of NF-κBp65.
{"title":"[Effects of Butylphthalide on the expressions of HMGB1 and RAGE in frontal lobe of rats after chronic sleep deprivation].","authors":"Ying-Xia Yang, Yu-Fen Guo, Hong-Hong Huang, Ling-Xing Wang","doi":"10.12047/j.cjap.6269.2022.090","DOIUrl":"https://doi.org/10.12047/j.cjap.6269.2022.090","url":null,"abstract":"<p><strong>Objective: </strong>To investigate the effects of Butylphthalide on the expressions of HMGB1 and RAGE in frontal lobe of rats after chronic sleep deprivation.</p><p><strong>Methods: </strong>Chronic sleep deprivation and butylphthalide treatment was performed in Sprague Dawley(SD)rats and the rats were divided into three groups (<i>n</i>=6): platform control group, chronic sleep deprivation group and chronic sleep deprivation + butylphthalide intervention group. Rats suffering chronic sleep deprivation were put in multiple platforms box for 18 h per day and sleep deprivation lasted for 28 days. Rats in butylphthalide intervention group were intraperitoneally injected with butylphthalide 100 mg/(kg·d) for 14 days after sleep deprivation. After collecting brains, high-mobility group box (HMGB1) and nuclear transcription factor kappB (NF-κB)p65 were detected by immunohistochemistry. The expression of HMGB1, silent information regulator of transcription 1 (SIRT1), receptor for advanced glycation end-products (RAGE) and NF-κB in frontal lobe were determinated by Western blot.</p><p><strong>Results: </strong>Compared with platform control group, the expression levels of HMGB1, RAGE and nuclear NF-κB p65 were increased significantly, while the expression of SIRT1 was decreased siginificantly in frontal lobe of chronic sleep deprivation group (all <i>P</i><0.05). Compared with chronic sleep deprivation group, the expression levels of of HMGB1, RAGE and nuclear NF-κB p65 were decreased significantly, while the expression of SIRT1 was increased significantly in chronic sleep deprivation + butylphthalide intervention group (all <i>P</i><0.05).</p><p><strong>Conclusion: </strong>Butylphthalide can inhibit HMGB1/RAGE/NF-κB pathway in frontal lobe of rats after chronic sleep deprivation by changing the expression of HMGB1 and RAGE, and reducing the nuclear translocation of NF-κBp65.</p>","PeriodicalId":23985,"journal":{"name":"Zhongguo ying yong sheng li xue za zhi = Zhongguo yingyong shenglixue zazhi = Chinese journal of applied physiology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2022-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9423081","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Objective: To investigate the effects of blocking lactate synthesis on the HT22 cell injuries caused by hypoxia.
Methods: 2-deoxy-D-glucose (2-DG) is a non-metabolized glucose analogue that can inhibit lactate synthesis by blocking glycolysis. HT22 cells were divided into 4 groups: Control group, 2-DG group, Hypoxia group and 2-DG+Hypoxia group. The cells in control group and 2-DG treatment group were cultured in a 37℃, 5% CO2 incubator, and thecells in hypoxia group and 2-DG + Hypoxia group were cultured in a hypoxia incubator. The concentrations of 2-DG were 2.5 and 5 mmol/L, the concentration of oxygen was 0.3%, and the treatment time was 24 h. Cell activity was detected by CCK-8 assay, the levels of lactate in cell culture medium were detected by spectrophotometry, cell morphology was observed by fluorescence staining, the level of reactive oxygen species (ROS) was detected by flow cytometry, and the activities of superoxide dismutase (SOD) and catalase (CAT) were determined by enzyme activity kits. The protein expression levels of p-p38, t-p38 and β-actin were detected by Western blot.
Results: Compared with that in control group, the lactate level in culture medium and cell activity were decreased significantly (P<0.01), the number of adherent cells was decreased, the level of ROS was increased (P<0.01), and the enzyme activity of CAT was decreased (P<0.05) in the 2-DG group. In the hypoxia group, the level of lactate in the culture medium was increased significantly (P<0.01), the cell activity was decreased (P<0.01), the number of adherent cells was decreased, the ROS levels were increased (P<0.01), and the enzyme activities of CAT and SOD were decreased (P<0.01 or P<0.05). In 2-DG+Hypoxia group, the level of lactate was decreased significantly (P<0.05), the cell viability was decreased significantly (P<0.01), the number of cells was decreased significantly, and the ability of adhere to the wall was weakened significantly. The level of ROS was increased significantly (P<0.01), the enzyme activities of CAT and SOD were decreased significantly (P<0.01), the protein expression level of p-p38 was increased significantly (P<0.05), and there was no change in t-p38. Compared with hypoxia groups, in 2-DG combined with hypoxia group, the level of lactate induced by hypoxia, the cell activity, and the enzyme activity level of CAT were decreased significantly (all P<0.01), while the level of ROS was increased significantly (P< 0.01).
Conclusion: Blocking lactate can reduce the cell activity level under hypoxia and aggravate the oxidative stress injury of HT22 cells. The mechanisms may be related to increasing ROS level and activating p38 signal pathway.
{"title":"[Effects of blocking lactate production by 2-DG on hypoxic injury of HT22 neurons and its mechanisms].","authors":"Yue Hu, Zi-Bi Shi, Qian-Qian Ruan, Ya-Nan Geng, Xiang Cheng, Ming Zhao, Ling-Ling Zhu","doi":"10.12047/j.cjap.6276.2022.075","DOIUrl":"https://doi.org/10.12047/j.cjap.6276.2022.075","url":null,"abstract":"<p><strong>Objective: </strong>To investigate the effects of blocking lactate synthesis on the HT22 cell injuries caused by hypoxia.</p><p><strong>Methods: </strong>2-deoxy-D-glucose (2-DG) is a non-metabolized glucose analogue that can inhibit lactate synthesis by blocking glycolysis. HT22 cells were divided into 4 groups: Control group, 2-DG group, Hypoxia group and 2-DG+Hypoxia group. The cells in control group and 2-DG treatment group were cultured in a 37℃, 5% CO<sub>2</sub> incubator, and thecells in hypoxia group and 2-DG + Hypoxia group were cultured in a hypoxia incubator. The concentrations of 2-DG were 2.5 and 5 mmol/L, the concentration of oxygen was 0.3%, and the treatment time was 24 h. Cell activity was detected by CCK-8 assay, the levels of lactate in cell culture medium were detected by spectrophotometry, cell morphology was observed by fluorescence staining, the level of reactive oxygen species (ROS) was detected by flow cytometry, and the activities of superoxide dismutase (SOD) and catalase (CAT) were determined by enzyme activity kits. The protein expression levels of p-p38, t-p38 and β-actin were detected by Western blot.</p><p><strong>Results: </strong>Compared with that in control group, the lactate level in culture medium and cell activity were decreased significantly (<i>P</i><0.01), the number of adherent cells was decreased, the level of ROS was increased (<i>P</i><0.01), and the enzyme activity of CAT was decreased (<i>P</i><0.05) in the 2-DG group. In the hypoxia group, the level of lactate in the culture medium was increased significantly (<i>P</i><0.01), the cell activity was decreased (<i>P</i><0.01), the number of adherent cells was decreased, the ROS levels were increased (<i>P</i><0.01), and the enzyme activities of CAT and SOD were decreased (<i>P</i><0.01 or <i>P</i><0.05). In 2-DG+Hypoxia group, the level of lactate was decreased significantly (<i>P</i><0.05), the cell viability was decreased significantly (<i>P</i><0.01), the number of cells was decreased significantly, and the ability of adhere to the wall was weakened significantly. The level of ROS was increased significantly (<i>P</i><0.01), the enzyme activities of CAT and SOD were decreased significantly (<i>P</i><0.01), the protein expression level of p-p38 was increased significantly (<i>P</i><0.05), and there was no change in t-p38. Compared with hypoxia groups, in 2-DG combined with hypoxia group, the level of lactate induced by hypoxia, the cell activity, and the enzyme activity level of CAT were decreased significantly (all <i>P</i><0.01), while the level of ROS was increased significantly (<i>P</i>< 0.01).</p><p><strong>Conclusion: </strong>Blocking lactate can reduce the cell activity level under hypoxia and aggravate the oxidative stress injury of HT22 cells. The mechanisms may be related to increasing ROS level and activating p38 signal pathway.</p>","PeriodicalId":23985,"journal":{"name":"Zhongguo ying yong sheng li xue za zhi = Zhongguo yingyong shenglixue zazhi = Chinese journal of applied physiology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2022-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9424813","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Objective: To investigate the mechanisms of Astragaloside Ⅳ on inhibiting apoptosis and delaying kidney aging in rats by regulating SIRT1/p53 signaling pathway.
Methods: The aging model was established by subcutaneous injection of D-galactose 200 mg/(kg·d). SPF-grade healthy male SD rats were randomly divided into 4 groups: normal control group (intragastric infusion of 5 ml/(kg·d) normal saline), aging model group (intragastric infusion of 5 ml/(kg·d) normal saline), Astragaloside IV group (intragastric infusion of 40 mg/(kg·d) Astragaloside IV),and SRT1720 group( intragastric infusion of 20 mg/(kg·d) SRT1720), with 10 rats in each group. After 8 weeks, the serum samples of rats were collected to detect the levels of renal function (creatinine and urea nitrogen) and senescent associated secretory phenotype (TGF-β and IL-6) by ELISA. The renal tissues of rats were obtained for HE and Masson staining. The protein and mRNA expressions of SIRT1, p53, Bcl-2, Bax, p21 and pRb were detected by Western blot and RT-PCR.
Results: Serum creatinine and urea nitrogen levels in the aging model group were higher than those in the normal group, but there was no significant difference in each group (P>0.05). The serum levels of TGF-β and IL-6 in the aging model group were higher than those in the normal group (P<0.05), and which in the Astragaloside IV group and SRT1720 group were lower than those in the model group (P<0.05). There was no significant differences between Astragaloside IV group and SRT1720 group (P>0.05). The results of pathological staining of renal tissues showed that, compared with the normal group, the renal tubules dilated, local atrophy, infiltration of inflammatory cells and proliferation of collagen fibers were observed in the aging model group. Compared with the aging model group, the pathological changes were alleviated in Astragaloside IV group and SRT1720 group. The results of Western blot and RT-PCR showed that, compared with the normal group, the protein and mRNA expressions of SIRT1 and pRb in the renal tissue of the aging group were decreased, the protein expression of Bcl-2 was decreased(P<0.05), and the protein and mRNA expressions of p53 and p21 were increased, the protein expression of Bax was increased(P<0.05). Compared with the aging group, Astragaloside IV and SRT1720 improved the above-mentioned indexes (P<0.05).
Conclusion: Astragaloside IV can delay kidney aging by regulating the SIRT1/p53 signaling pathway.
{"title":"[Effects of astragaloside IV on delaying kidney aging and its mechanisms].","authors":"Zi-Yuan Zhang, Jing-Ai Fang, Su-Fen Li, Ya-Ling Hu, Wen-Yuan Liu, Xue-Jun Liu","doi":"10.12047/j.cjap.6300.2022.084","DOIUrl":"https://doi.org/10.12047/j.cjap.6300.2022.084","url":null,"abstract":"<p><strong>Objective: </strong>To investigate the mechanisms of Astragaloside Ⅳ on inhibiting apoptosis and delaying kidney aging in rats by regulating SIRT1/p53 signaling pathway.</p><p><strong>Methods: </strong>The aging model was established by subcutaneous injection of D-galactose 200 mg/(kg·d). SPF-grade healthy male SD rats were randomly divided into 4 groups: normal control group (intragastric infusion of 5 ml/(kg·d) normal saline), aging model group (intragastric infusion of 5 ml/(kg·d) normal saline), Astragaloside IV group (intragastric infusion of 40 mg/(kg·d) Astragaloside IV),and SRT1720 group( intragastric infusion of 20 mg/(kg·d) SRT1720), with 10 rats in each group. After 8 weeks, the serum samples of rats were collected to detect the levels of renal function (creatinine and urea nitrogen) and senescent associated secretory phenotype (TGF-β and IL-6) by ELISA. The renal tissues of rats were obtained for HE and Masson staining. The protein and mRNA expressions of SIRT1, p53, Bcl-2, Bax, p21 and pRb were detected by Western blot and RT-PCR.</p><p><strong>Results: </strong>Serum creatinine and urea nitrogen levels in the aging model group were higher than those in the normal group, but there was no significant difference in each group (<i>P</i>>0.05). The serum levels of TGF-β and IL-6 in the aging model group were higher than those in the normal group (<i>P</i><0.05), and which in the Astragaloside IV group and SRT1720 group were lower than those in the model group (<i>P</i><0.05). There was no significant differences between Astragaloside IV group and SRT1720 group (<i>P</i>>0.05). The results of pathological staining of renal tissues showed that, compared with the normal group, the renal tubules dilated, local atrophy, infiltration of inflammatory cells and proliferation of collagen fibers were observed in the aging model group. Compared with the aging model group, the pathological changes were alleviated in Astragaloside IV group and SRT1720 group. The results of Western blot and RT-PCR showed that, compared with the normal group, the protein and mRNA expressions of SIRT1 and pRb in the renal tissue of the aging group were decreased, the protein expression of Bcl-2 was decreased(<i>P</i><0.05), and the protein and mRNA expressions of p53 and p21 were increased, the protein expression of Bax was increased(<i>P</i><0.05). Compared with the aging group, Astragaloside IV and SRT1720 improved the above-mentioned indexes (<i>P</i><0.05).</p><p><strong>Conclusion: </strong>Astragaloside IV can delay kidney aging by regulating the SIRT1/p53 signaling pathway.</p>","PeriodicalId":23985,"journal":{"name":"Zhongguo ying yong sheng li xue za zhi = Zhongguo yingyong shenglixue zazhi = Chinese journal of applied physiology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2022-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9424818","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2022-09-01DOI: 10.12047/j.cjap.6289.2022.082
Wen-Yu Zeng, Wen-Yan Gu, Li Xyu, Ying Zhang, Cong Han
Objective: To study the effects of miR-99b-5p (non-coding RNA) in alleviating pathological neuropathic pain after paclitaxel chemotherapy by inhibiting NLRP3 inflammatory vesicle activation and the effects on neuronal cells pyrosis and apoptosis.
Methods: SD rats were randomly divided into blank group, model group, agomiR-99b-5P treatment group, and agomiR-NC group, 6 rats in each group. The blank group received saline treatment as a control, the model group established a pain model induced by paclitaxel, and the rats in agomiR-99b-5p treatment group and agomiR-NC group were treated with agomiR-99b-5p and agomiR-NC injections, respectively. The expressions of miR-99b-5p in the blank group, model group, and treatment group were detected by RT-qPCR. The mechanical foot retraction threshold (MWT) of the blank group, model group, and treatment group were detected. TUNEL was used to detect the apoptosis of spinal dorsal horn cells. The levels of ROS, MDA, and SOD were detected by ELISA kits. The protein expressions of NLRP3, caspase-1, and IL-1β were detected by immunofluorescence staining.
Results: Compared with the model group, the expression level of miR-99b-5p and the MWT were increased significantly in agomiR-99b-5p treatment group (P<0.05), the apoptosis of dorsal horn cells was inhibited (P<0.05), the level of antioxidant stress was increased in rats, the levels of ROS and MDA were decreased (P<0.05), while the level of SOD was increased (P<0.05). Immunofluorescence showed that the expressions of NLRP3, caspase-1, and IL-1β were inhibited by miR-99b-5p.
Conclusion: miR-99b-5p can alleviate the apoptosis and pyroptosis of neurons after paclitaxel chemotherapy by inhibiting the activation of NLRP3 and improving oxidative stress in vivo.
{"title":"[miR-99b-5p inhibits the activation of NLRP3 inflammasome to alleviate the neurotoxicity induced by paclitaxel chemotherapy].","authors":"Wen-Yu Zeng, Wen-Yan Gu, Li Xyu, Ying Zhang, Cong Han","doi":"10.12047/j.cjap.6289.2022.082","DOIUrl":"https://doi.org/10.12047/j.cjap.6289.2022.082","url":null,"abstract":"<p><strong>Objective: </strong>To study the effects of miR-99b-5p (non-coding RNA) in alleviating pathological neuropathic pain after paclitaxel chemotherapy by inhibiting NLRP3 inflammatory vesicle activation and the effects on neuronal cells pyrosis and apoptosis.</p><p><strong>Methods: </strong>SD rats were randomly divided into blank group, model group, agomiR-99b-5P treatment group, and agomiR-NC group, 6 rats in each group. The blank group received saline treatment as a control, the model group established a pain model induced by paclitaxel, and the rats in agomiR-99b-5p treatment group and agomiR-NC group were treated with agomiR-99b-5p and agomiR-NC injections, respectively. The expressions of miR-99b-5p in the blank group, model group, and treatment group were detected by RT-qPCR. The mechanical foot retraction threshold (MWT) of the blank group, model group, and treatment group were detected. TUNEL was used to detect the apoptosis of spinal dorsal horn cells. The levels of ROS, MDA, and SOD were detected by ELISA kits. The protein expressions of NLRP3, caspase-1, and IL-1β were detected by immunofluorescence staining.</p><p><strong>Results: </strong>Compared with the model group, the expression level of miR-99b-5p and the MWT were increased significantly in agomiR-99b-5p treatment group (<i>P</i><0.05), the apoptosis of dorsal horn cells was inhibited (<i>P</i><0.05), the level of antioxidant stress was increased in rats, the levels of ROS and MDA were decreased (<i>P</i><0.05), while the level of SOD was increased (<i>P</i><0.05). Immunofluorescence showed that the expressions of NLRP3, caspase-1, and IL-1β were inhibited by miR-99b-5p.</p><p><strong>Conclusion: </strong>miR-99b-5p can alleviate the apoptosis and pyroptosis of neurons after paclitaxel chemotherapy by inhibiting the activation of NLRP3 and improving oxidative stress <i>in vivo.</i></p>","PeriodicalId":23985,"journal":{"name":"Zhongguo ying yong sheng li xue za zhi = Zhongguo yingyong shenglixue zazhi = Chinese journal of applied physiology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2022-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9428313","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2022-09-01DOI: 10.12047/j.cjap.6278.2022.045
Yu Jiao Zhang, Tong Shi, Ting Li, Xiang Chen Dang, Jun Yu Lu, Xue Wei Chen, Qiang Ma
目的: 分析不同海拔高原人群在递增负荷运动情况下的通气量与心率的变化特征,探讨其作为高原体力劳动强度分级评价指标的可行性。方法: 选取高原习服男性青年军人88名,平均年龄21.7±1.6。其中3 000 m 30人,3 700 m 30人,4 300 m 28人,进行递增负荷踏车运动,运动负荷从30 W开始,每5 min增加30 W,直到不能坚持则停止运动。采用COSMED K5运动肺功能仪测量每一运动负荷的肺通气量,POLAR V800心率表测量每一运动负荷的运动心率。结果: 不同海拔递增负荷运动中完成最大负荷的人数具有显著差异(P<0.05),海拔越高,完成人数越少。同一海拔,不同负荷之间,随着负荷的增加,通气量与心率明显增大(P<0.05),且无上限值;同一负荷,随海拔增加,通气量与心率也明显增大(P<0.05)。结论: 通气量与心率具有作为高原体力劳动强度分级评价指标的可行性。.
{"title":"[Effects of incremental exercise on ventilation and heart rates of people at different altitudes].","authors":"Yu Jiao Zhang, Tong Shi, Ting Li, Xiang Chen Dang, Jun Yu Lu, Xue Wei Chen, Qiang Ma","doi":"10.12047/j.cjap.6278.2022.045","DOIUrl":"https://doi.org/10.12047/j.cjap.6278.2022.045","url":null,"abstract":"目的: 分析不同海拔高原人群在递增负荷运动情况下的通气量与心率的变化特征,探讨其作为高原体力劳动强度分级评价指标的可行性。方法: 选取高原习服男性青年军人88名,平均年龄21.7±1.6。其中3 000 m 30人,3 700 m 30人,4 300 m 28人,进行递增负荷踏车运动,运动负荷从30 W开始,每5 min增加30 W,直到不能坚持则停止运动。采用COSMED K5运动肺功能仪测量每一运动负荷的肺通气量,POLAR V800心率表测量每一运动负荷的运动心率。结果: 不同海拔递增负荷运动中完成最大负荷的人数具有显著差异(P<0.05),海拔越高,完成人数越少。同一海拔,不同负荷之间,随着负荷的增加,通气量与心率明显增大(P<0.05),且无上限值;同一负荷,随海拔增加,通气量与心率也明显增大(P<0.05)。结论: 通气量与心率具有作为高原体力劳动强度分级评价指标的可行性。.","PeriodicalId":23985,"journal":{"name":"Zhongguo ying yong sheng li xue za zhi = Zhongguo yingyong shenglixue zazhi = Chinese journal of applied physiology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2022-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40351741","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2022-09-01DOI: 10.12047/j.cjap.6312.2022.098
Xuan Qiu, Lei Yu, Si-Yu Tian, Ya-Jie Chen, Hong-Ling Yan, Kuan-Zhi Liu
Objective: To investigate the effect of α-lipoic acid in ameliorating liver injury in rats with type 2 diabetes mellitus via activating adenosine 5'-monophosphate-activate protein kinase (AMPK)/mammalian target of rapamycin (mTOR) pathway.
Methods: The T2DM rat models were established by feeding with high-fat, high-sucrose diet and intraperitoneal injection of 27.5 mg/(kg·d) streptozotocin. The 32 rats with T2DM were randomly divided into 4 groups: T2DM group, α-lipoic acid group (LA), Compound C group (Comp C, an inhibitor of AMPK) and LA+Comp C group, with 8 rats in each group. Additionally, 8 Sprague-Dawlay (SD) rats without diabetes were set as normal control. The rats received α-lipoic acid at a dosage of 100 mg/(kg·d) or Compound C at a dosage of 20 mg/(kg·d) by intraperitoneal injection for 8 weeks as needed. The levels of relevant biochemical indexes were detected. The weight of liver was recorded to calculate liver weight index (LWI), and the pathological changes of liver tissues were detected by light and electron microscopy. The levels of AMPK, p-AMPK, mTOR, p-mTOR in rat liver were detected by Western blot.
Results: Compared with control group, the levels of LWI, homeostasis model assessment of insulin resistance, fasting blood glucose, alanine transaminase, aspartate transaminase, gamma glutamyl transferase and triglyceride in T2DM group were increased significantly (all P<0.05). The liver tissue lesions were more serious and hepatic steatosis grade was higher. The expression of p-AMPK was decreased (P<0.05) and the expression of p-mTOR was increased significantly(P<0.05). α-lipoic acid could reverse the above-mentioned changes, ameliorate insulin resistance (all P<0.05), protect the structure and function of liver, and activate the AMPK/mTOR pathway (P<0.05). The protection of α-lipoic acid was weakened by the inhibition of AMPK with Compound C (P<0.05).
Conclusion: α-lipoic acid could protect the liver of rats with T2DM by activating AMPK/mTOR pathway.
{"title":"[α-lipoic acid ameliorates liver injury in rats with type 2 diabetes mellitus <i>via</i> activating AMPK/mTOR pathway].","authors":"Xuan Qiu, Lei Yu, Si-Yu Tian, Ya-Jie Chen, Hong-Ling Yan, Kuan-Zhi Liu","doi":"10.12047/j.cjap.6312.2022.098","DOIUrl":"https://doi.org/10.12047/j.cjap.6312.2022.098","url":null,"abstract":"<p><strong>Objective: </strong>To investigate the effect of α-lipoic acid in ameliorating liver injury in rats with type 2 diabetes mellitus <i>via</i> activating adenosine 5'-monophosphate-activate protein kinase (AMPK)/mammalian target of rapamycin (mTOR) pathway.</p><p><strong>Methods: </strong>The T2DM rat models were established by feeding with high-fat, high-sucrose diet and intraperitoneal injection of 27.5 mg/(kg·d) streptozotocin. The 32 rats with T2DM were randomly divided into 4 groups: T2DM group, α-lipoic acid group (LA), Compound C group (Comp C, an inhibitor of AMPK) and LA+Comp C group, with 8 rats in each group. Additionally, 8 Sprague-Dawlay (SD) rats without diabetes were set as normal control. The rats received α-lipoic acid at a dosage of 100 mg/(kg·d) or Compound C at a dosage of 20 mg/(kg·d) by intraperitoneal injection for 8 weeks as needed. The levels of relevant biochemical indexes were detected. The weight of liver was recorded to calculate liver weight index (LWI), and the pathological changes of liver tissues were detected by light and electron microscopy. The levels of AMPK, p-AMPK, mTOR, p-mTOR in rat liver were detected by Western blot.</p><p><strong>Results: </strong>Compared with control group, the levels of LWI, homeostasis model assessment of insulin resistance, fasting blood glucose, alanine transaminase, aspartate transaminase, gamma glutamyl transferase and triglyceride in T2DM group were increased significantly (all <i>P</i><0.05). The liver tissue lesions were more serious and hepatic steatosis grade was higher. The expression of p-AMPK was decreased (<i>P</i><0.05) and the expression of p-mTOR was increased significantly(<i>P</i><0.05). α-lipoic acid could reverse the above-mentioned changes, ameliorate insulin resistance (all <i>P</i><0.05), protect the structure and function of liver, and activate the AMPK/mTOR pathway (<i>P</i><0.05). The protection of α-lipoic acid was weakened by the inhibition of AMPK with Compound C (<i>P</i><0.05).</p><p><strong>Conclusion: </strong>α-lipoic acid could protect the liver of rats with T2DM by activating AMPK/mTOR pathway.</p>","PeriodicalId":23985,"journal":{"name":"Zhongguo ying yong sheng li xue za zhi = Zhongguo yingyong shenglixue zazhi = Chinese journal of applied physiology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2022-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9423078","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2022-09-01DOI: 10.12047/j.cjap.6270.2022.088
Xiao-Hong Gou, Xue-Nong He, Shi-Shuang Jiang, Wu Tao, Chao-Hui He
Objective: To investigate the effects of glucocorticoid receptor agonists on hyperalgesia in rats with neuropathic pain (NPP) by regulating nucleotide-binding oligomerization domain-like receptor protein 3 (NLRP3)/interleukin-1β (IL-1β) pathway and its mechanisms.
Methods: Forty SD rats were divided into control group, NPP model group, NPP treated with NLRP3 inhibitor group and dexamethasone treatment group with 10 rats in each group. The NPP rat model was induced by vincristine. The model group was established according to the above method, the NLRP3 inhibitor group was treated with NLRP3 inhibitor (MCC950) after the NPP model was established, and the treatment group was treated with glucocorticoid receptor agonist (dexamethasone) after the model was established according to the design. The rats of the control group were given the same amount of normal saline. After 7 days of intervention, the mechanical pain threshold, thermal pain threshold, morphological changes of spinal dorsal horn, pain factors (prostaglandin E2 (PGE2), substance P (SP), 5-hydroxytryptamine (5-HT)), inflammatory factors (interleukin-8 (IL-8), tumor necrosis factor α (TNF-α), interleukin-6 (IL-6)), and NLRP3/IL-1β protein expressions were determined and compared among the four groups.
Results: Compared with the model group, the pathological changes of spinal dorsal horn neurons in NLRP3 inhibitor group and treatment group were alleviated significantly, the arrangement of neurons was tended to be close, the number of neurons was gradually returned to normal, and the pyknosis of neurons was decreased. Compared with the control group, the mechanical pain threshold and thermal pain threshold of the model group were decreased significantly (P<0.05), and the expressions of inflammatory factors, pain factors and NLRP3, IL-1β protein were increased significantly (P<0.05); compared with the model group, the mechanical pain threshold and thermal pain threshold of the NLRP3 inhibitor group and the dexamethasone treatment group were increased significantly (P<0.05), and the expressions of inflammatory factors, pain factors and NLRP3, IL-1β protein were decreased significantly (P< 0.05). The difference between NLRP3 inhibitor group and treatment group was not statistically significant (P>0.05).
Conclusion: Glucocorticoid receptor agonists may reduce the hyperalgesia of neuropathic pain rat model by down regulating NLRP3/IL-1β pathway, which may be the mechanism of dexamethasone on antiinflammatory of analgesia in early stage of NPP.
{"title":"[Effects of glucocorticoid receptor agonists on hyperalgesia of rats with neuropathic pain and its mechanisms].","authors":"Xiao-Hong Gou, Xue-Nong He, Shi-Shuang Jiang, Wu Tao, Chao-Hui He","doi":"10.12047/j.cjap.6270.2022.088","DOIUrl":"https://doi.org/10.12047/j.cjap.6270.2022.088","url":null,"abstract":"<p><strong>Objective: </strong>To investigate the effects of glucocorticoid receptor agonists on hyperalgesia in rats with neuropathic pain (NPP) by regulating nucleotide-binding oligomerization domain-like receptor protein 3 (NLRP3)/interleukin-1β (IL-1β) pathway and its mechanisms.</p><p><strong>Methods: </strong>Forty SD rats were divided into control group, NPP model group, NPP treated with NLRP3 inhibitor group and dexamethasone treatment group with 10 rats in each group. The NPP rat model was induced by vincristine. The model group was established according to the above method, the NLRP3 inhibitor group was treated with NLRP3 inhibitor (MCC950) after the NPP model was established, and the treatment group was treated with glucocorticoid receptor agonist (dexamethasone) after the model was established according to the design. The rats of the control group were given the same amount of normal saline. After 7 days of intervention, the mechanical pain threshold, thermal pain threshold, morphological changes of spinal dorsal horn, pain factors (prostaglandin E2 (PGE2), substance P (SP), 5-hydroxytryptamine (5-HT)), inflammatory factors (interleukin-8 (IL-8), tumor necrosis factor α (TNF-α), interleukin-6 (IL-6)), and NLRP3/IL-1β protein expressions were determined and compared among the four groups.</p><p><strong>Results: </strong>Compared with the model group, the pathological changes of spinal dorsal horn neurons in NLRP3 inhibitor group and treatment group were alleviated significantly, the arrangement of neurons was tended to be close, the number of neurons was gradually returned to normal, and the pyknosis of neurons was decreased. Compared with the control group, the mechanical pain threshold and thermal pain threshold of the model group were decreased significantly (<i>P</i><0.05), and the expressions of inflammatory factors, pain factors and NLRP3, IL-1β protein were increased significantly (<i>P</i><0.05); compared with the model group, the mechanical pain threshold and thermal pain threshold of the NLRP3 inhibitor group and the dexamethasone treatment group were increased significantly (<i>P</i><0.05), and the expressions of inflammatory factors, pain factors and NLRP3, IL-1β protein were decreased significantly (<i>P</i>< 0.05). The difference between NLRP3 inhibitor group and treatment group was not statistically significant (<i>P</i>>0.05).</p><p><strong>Conclusion: </strong>Glucocorticoid receptor agonists may reduce the hyperalgesia of neuropathic pain rat model by down regulating NLRP3/IL-1β pathway, which may be the mechanism of dexamethasone on antiinflammatory of analgesia in early stage of NPP.</p>","PeriodicalId":23985,"journal":{"name":"Zhongguo ying yong sheng li xue za zhi = Zhongguo yingyong shenglixue zazhi = Chinese journal of applied physiology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2022-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9423080","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Objective: To study the effects of octadecadienoic acid (ODA) on the proliferation and apoptosis of glioma cells and its mechanisms.
Methods: Cultured human glioma cells (cell density 2×106 cells/L) were divided into solvent control group (DMSO, 30 μl/L), 5-FU group (10 mg/L) and octadecadienic acid groups (0.3, 0.6 and 1.2 mg/L groups). The toxicity of ODA on glioma cells was detected by trypan blue and thiazolium blue (MTT). The expression levels of P53, PI3K, P21, PKB/Akt and Caspase-9 in glioma cells were determined by enzyme-linked immunosorbent assay (ELISA).
Results: ① Cell count under optical microscope showed that the inhibition rate of cell proliferation in ODA low, medium and high dose groups and 5-FU group was significantly higher than that in the solvent control group (P<0.01), but there was no statistical significance compared with the 5-FU group (P>0.05). ② MTT assay showed that the inhibition rate of cell proliferation was increased significantly in ODA low, medium and high dose groups and 5-FU groups (P<0.01), compared with the solvent control group. Compared with 5-FU group, the inhibition rate of cell proliferation was increased significantly only in ODA high dose group (P<0.01). ③ The number of G0/G1 phase cells in ODA low, medium and high dose groups and 5-FU group were increased significantly (P<0.05, P<0.01), the number of G2/M phase cells were decreased significantly (P<0.01), and the apoptosis rate was increased significantly (P<0.01),compared with the solvent control group. Compared with the 5-FU group, the number of cells in G2/M phase was decreased significantly (P<0.01) and the apoptosis rate was increased significantly (P<0.01) in ODA high dose group. ④ ELISA test results showed that the protein expression levels of P53, PI3K and PKB/Akt in ODA low , medium and high dose groups and 5-FU group were significantly lower than those in solvent control group (all P<0.01), but the protein expression levels in ODA high dose group were significantly lower than those in 5-FU group (P<0.01). The protein expression levels of P21 and caspase-9 in ODA low , medium and high dose groups and 5-FU group were significantly higher than those in solvent control group (P<0.05, P<0.01), but the protein expression levels in ODA high dose group were significantly higher than those in 5-Fu group (P<0.01).
Conclusion: ODA can significantly inhibit the proliferation and promote apoptosis of glioma cells. The mechanisms are related to up-regulating the levels of P21 and caspase-9 to promote apoptosis, down-regulating the levels of P53, PI3K and PKB/Akt to inhibit the cell division cycle, and reducing the activity of PI3K-Akt signal transduction pathway.
{"title":"[Effects of octadecadienoic acid on proliferation and apoptosis of glioma cells and its mechanisms].","authors":"Ming-Ren Xie, Tian-Xiao He, Xia Yuan, Jing Zhang, Lei Yu, Fa-Rong Yu","doi":"10.12047/j.cjap.6271.2022.081","DOIUrl":"https://doi.org/10.12047/j.cjap.6271.2022.081","url":null,"abstract":"<p><strong>Objective: </strong>To study the effects of octadecadienoic acid (ODA) on the proliferation and apoptosis of glioma cells and its mechanisms.</p><p><strong>Methods: </strong>Cultured human glioma cells (cell density 2×10<sup>6</sup> cells/L) were divided into solvent control group (DMSO, 30 μl/L), 5-FU group (10 mg/L) and octadecadienic acid groups (0.3, 0.6 and 1.2 mg/L groups). The toxicity of ODA on glioma cells was detected by trypan blue and thiazolium blue (MTT). The expression levels of P53, PI3K, P21, PKB/Akt and Caspase-9 in glioma cells were determined by enzyme-linked immunosorbent assay (ELISA).</p><p><strong>Results: </strong>① Cell count under optical microscope showed that the inhibition rate of cell proliferation in ODA low, medium and high dose groups and 5-FU group was significantly higher than that in the solvent control group (<i>P</i><0.01), but there was no statistical significance compared with the 5-FU group (<i>P</i>>0.05). ② MTT assay showed that the inhibition rate of cell proliferation was increased significantly in ODA low, medium and high dose groups and 5-FU groups (<i>P</i><0.01), compared with the solvent control group. Compared with 5-FU group, the inhibition rate of cell proliferation was increased significantly only in ODA high dose group (<i>P</i><0.01). ③ The number of G<sub>0</sub>/G<sub>1</sub> phase cells in ODA low, medium and high dose groups and 5-FU group were increased significantly (<i>P</i><0.05, <i>P</i><0.01), the number of G<sub>2</sub>/M phase cells were decreased significantly (<i>P</i><0.01), and the apoptosis rate was increased significantly (<i>P</i><0.01),compared with the solvent control group. Compared with the 5-FU group, the number of cells in G<sub>2</sub>/M phase was decreased significantly (<i>P</i><0.01) and the apoptosis rate was increased significantly (<i>P</i><0.01) in ODA high dose group. ④ ELISA test results showed that the protein expression levels of P53, PI3K and PKB/Akt in ODA low , medium and high dose groups and 5-FU group were significantly lower than those in solvent control group (all <i>P</i><0.01), but the protein expression levels in ODA high dose group were significantly lower than those in 5-FU group (<i>P</i><0.01). The protein expression levels of P21 and caspase-9 in ODA low , medium and high dose groups and 5-FU group were significantly higher than those in solvent control group (<i>P</i><0.05, <i>P</i><0.01), but the protein expression levels in ODA high dose group were significantly higher than those in 5-Fu group (<i>P</i><0.01).</p><p><strong>Conclusion: </strong>ODA can significantly inhibit the proliferation and promote apoptosis of glioma cells. The mechanisms are related to up-regulating the levels of P21 and caspase-9 to promote apoptosis, down-regulating the levels of P53, PI3K and PKB/Akt to inhibit the cell division cycle, and reducing the activity of PI3K-Akt signal transduction pathway.</p>","PeriodicalId":23985,"journal":{"name":"Zhongguo ying yong sheng li xue za zhi = Zhongguo yingyong shenglixue zazhi = Chinese journal of applied physiology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2022-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9428308","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2022-09-01DOI: 10.12047/j.cjap.6324.2022.102
Hang Xu, Ling Hu, Rong Jiang, Tao Zhang, Shuang He, Rui-Jing Lu, Jia-Ming He, Meng-Na Wu, Yue Sun, Jing Li, Jian-Hua Ran
Objective: To investigate the injury of cyanate on the pulmonary function and morphology of C57/BL6N mice.
Methods: Forty male C57/BL6N mice were randomly divided into two groups: normal control group (20 mice) and cyanate group (20 mice). Mice were exposed to 100 mmol/L cyanate feeding for 4 weeks, and pulmonary Raw (Resistance in Air Way) was measured at the beginning and end of the experiment. The mice were sacrificed at the end of the fourth week of the experiment, and the lung tissues were collected for pathological observation and molecular detection of E-Cadherin and Fibronectin. Well-growing A549 cells in logarithmic growth phase were treated with cyanate at the concentrations of 0, 0.25, 0.5 and 1 mmol/L for 24 h, and the cell viability was detected by CCK8 method; reactive oxygen species ROS fluorescent probe (DCFH-DA) was used to detect the changes of ROS levels, and expressions of E-Cadherin and Fibronectin in cells and pulmonary tissues were detected by Western blot.
Results: At the beginning of the experiment, the pulmonary airway resistance values of the mice in the normal control group and the cyanate group were (1.82±0.76)cmH2O/(L·s) and (1.85±0.78)cmH2O/(L·s), respectively, with no significant difference. Four weeks later, the pulmonary airway resistance value of mice in the cyanate group was increased to (4.86±0.87)cmH2O/(L·s) (P<0.01). The HE staining showed that, compared with the normal control group, the injured alveolar structure, the thickened tracheal wall and the significantly proliferated pulmonary interstitial tissue were observed in the cyanate group. The Masson staining showed that elastic fibers were deposited around the trachea of mice in the cyanate group. The results of CCK8 assay for the viability of A549 cells showed that 0.5 mmol/L cyanate exposure could reduce the viability (P<0.01). The immunofluorescence staining showed that cyanate could increase ROS level in A549 cells by producing green fluorescence in a concentration-dependent manner. The results of Western blotting showed that 0.5 mmol/L of cyanate treatment on A549 cells could reduce the expression of E-Cadherin (P<0.01) with increasing concentration of cyanate. The expression level of Fibronectin in A549 cells was increased with the increasing cyanate concentration, and there was a significant difference (P<0.01) on 1 mmol/L cyanate. Western blot results of lung showed the decreasing expression of E-Cadherin (P<0.01) and increasing expression of Fibronectin (P<0.01) in cyanate mice.
Conclusion: Pathological concentrations of cyanate can induce the proliferation of pulmonary interstitial tissue, fibrous deposition, and increased pulmonary airway resistance in mice, which may be related to damaged pulmonary epithelial cell viability, enhanced ROS production, and induced pathologic changes o
{"title":"[Effects of cyanate on pulmonary epithelial cells and pulmonary function in mice].","authors":"Hang Xu, Ling Hu, Rong Jiang, Tao Zhang, Shuang He, Rui-Jing Lu, Jia-Ming He, Meng-Na Wu, Yue Sun, Jing Li, Jian-Hua Ran","doi":"10.12047/j.cjap.6324.2022.102","DOIUrl":"https://doi.org/10.12047/j.cjap.6324.2022.102","url":null,"abstract":"<p><strong>Objective: </strong>To investigate the injury of cyanate on the pulmonary function and morphology of C57/BL6N mice.</p><p><strong>Methods: </strong>Forty male C57/BL6N mice were randomly divided into two groups: normal control group (20 mice) and cyanate group (20 mice). Mice were exposed to 100 mmol/L cyanate feeding for 4 weeks, and pulmonary Raw (Resistance in Air Way) was measured at the beginning and end of the experiment. The mice were sacrificed at the end of the fourth week of the experiment, and the lung tissues were collected for pathological observation and molecular detection of E-Cadherin and Fibronectin. Well-growing A549 cells in logarithmic growth phase were treated with cyanate at the concentrations of 0, 0.25, 0.5 and 1 mmol/L for 24 h, and the cell viability was detected by CCK8 method; reactive oxygen species ROS fluorescent probe (DCFH-DA) was used to detect the changes of ROS levels, and expressions of E-Cadherin and Fibronectin in cells and pulmonary tissues were detected by Western blot.</p><p><strong>Results: </strong>At the beginning of the experiment, the pulmonary airway resistance values of the mice in the normal control group and the cyanate group were (1.82±0.76)cmH<sub>2</sub>O/(L·s) and (1.85±0.78)cmH<sub>2</sub>O/(L·s), respectively, with no significant difference. Four weeks later, the pulmonary airway resistance value of mice in the cyanate group was increased to (4.86±0.87)cmH<sub>2</sub>O/(L·s) (<i>P</i><0.01). The HE staining showed that, compared with the normal control group, the injured alveolar structure, the thickened tracheal wall and the significantly proliferated pulmonary interstitial tissue were observed in the cyanate group. The Masson staining showed that elastic fibers were deposited around the trachea of mice in the cyanate group. The results of CCK8 assay for the viability of A549 cells showed that 0.5 mmol/L cyanate exposure could reduce the viability (<i>P</i><0.01). The immunofluorescence staining showed that cyanate could increase ROS level in A549 cells by producing green fluorescence in a concentration-dependent manner. The results of Western blotting showed that 0.5 mmol/L of cyanate treatment on A549 cells could reduce the expression of E-Cadherin (<i>P</i><0.01) with increasing concentration of cyanate. The expression level of Fibronectin in A549 cells was increased with the increasing cyanate concentration, and there was a significant difference (<i>P</i><0.01) on 1 mmol/L cyanate. Western blot results of lung showed the decreasing expression of E-Cadherin (<i>P</i><0.01) and increasing expression of Fibronectin (<i>P</i><0.01) in cyanate mice.</p><p><strong>Conclusion: </strong>Pathological concentrations of cyanate can induce the proliferation of pulmonary interstitial tissue, fibrous deposition, and increased pulmonary airway resistance in mice, which may be related to damaged pulmonary epithelial cell viability, enhanced ROS production, and induced pathologic changes o","PeriodicalId":23985,"journal":{"name":"Zhongguo ying yong sheng li xue za zhi = Zhongguo yingyong shenglixue zazhi = Chinese journal of applied physiology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2022-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9416157","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"[Effects of beta adrenergic receptor in hippocampal dentate gyrus on spatial learning and memory in sleep deprived rats and its mechanisms].","authors":"Jing Lyu, Cong Min Wang, Xin Liu, Ji Lin Yan","doi":"10.12047/j.cjap.6225.2022.048","DOIUrl":"https://doi.org/10.12047/j.cjap.6225.2022.048","url":null,"abstract":"目的: 探究海马齿状回(DG)内beta肾上腺素能受体(beta-AR)对睡眠剥夺(SD)大鼠空间学习记忆的作用及其机制。方法: 本研究应用剥夺杆式睡眠剥夺仪建立21 d(18 h/d)慢性SD模型。动物分为4组(n=6):对照组,ISO组(异丙肾上腺素组),SD组和SD+ISO组。每天训练前30 min,以0.5 ml/min速度向DG区微量注入ISO (2 mg/μl) 或盐水1 ml。Morris水迷宫检测大鼠空间学习记忆能力。免疫组织化学和免疫印迹法检测海马DG区c-Fos和脑源性神经营养因子(BDNF)表达。结果: 与对照组相比, SD组大鼠前4 d逃逸时间显著增加(P<0.01),且第5日目标象限时间比和穿台次数明显减少(P<0.05),与SD组相比SD+ISO组上述行为学指标显著改善(P均<0.05)。与对照组比较,SD组大鼠海马DG区c-Fos和BDNF蛋白表达水平均显著降低(P均<0.05),然而与SD组比较,SD+ISO组两蛋白表达水平明显增加(P均<0.05)。结论: 海马DG区beta-AR激活可改善SD诱发的空间学习和记忆障碍,其机制可能与上调DG区c-Fos和BDNF蛋白表达有关。.","PeriodicalId":23985,"journal":{"name":"Zhongguo ying yong sheng li xue za zhi = Zhongguo yingyong shenglixue zazhi = Chinese journal of applied physiology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2022-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40351658","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}