Background: The development and prognosis of breast cancer are intricately linked to psychological stress. In addition, depression is the most common psychological comorbidity among breast cancer survivors, and reportedly, Fang-Xia-Dihuang decoction (FXDH) can effectively manage depression in such patients. However, its pharmacological and molecular mechanisms remain obscure. Methods: Public databases were used for obtaining active components and related targets. Main active components were further verified by ultra-high-performance liquid chromatography-high-resolution mass spectrometry (UPLC-HRMS). Protein–protein interaction and enrichment analyses were taken to predict potential hub targets and related pathways. Molecule docking was used to understand the interactions between main compounds and hub targets. In addition, an animal model of breast cancer combined with depression was established to evaluate the intervention effect of FXDH and verify the pathways screened by network pharmacology. Results: 174 active components of FXDH and 163 intersection targets of FXDH, breast cancer, and depression were identified. Quercetin, methyl ferulate, luteolin, ferulaldehyde, wogonin, and diincarvilone were identified as the principal active components of FXDH. Protein–protein interaction and KEGG enrichment analyses revealed that the phosphoinositide-3-kinase–protein kinase B (PI3K/AKT) and Janus kinase/signal transducer and activator of transcription (JAK2/STAT3) signaling pathways played a crucial role in mediating the efficacy of FXDH for inhibiting breast cancer progression induced by depression. In addition, in vivo experiments revealed that FXDH ameliorated depression-like behavior in mice and inhibited excessive tumor growth in mice with breast cancer and depression. FXDH treatment downregulated the expression of epinephrine, PI3K, AKT, STAT3, and JAK2 compared with the control treatment (p < 0.05). Molecular docking verified the relationship between the six primary components of FXDH and the three most important targets, including phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha (PIK3CA), AKT, and STAT3. Conclusion: This study provides a scientific basis to support the clinical application of FXDH for improving depression-like behavior and inhibiting breast cancer progression promoted by chronic stress. The therapeutic effects FXDH may be closely related to the PI3K/AKT and JAK2/STAT3 pathways. This finding helps better understand the regulatory mechanisms underlying the efficacy of FXDH.
{"title":"Fang-Xia-Dihuang decoction inhibits breast cancer progression induced by psychological stress via down-regulation of PI3K/AKT and JAK2/STAT3 pathways: An in vivo and a network pharmacology assessment","authors":"LINGYAN LV, JING ZHAO, XUAN WANG, LIUYAN XU, YINGYI FAN, CHUNHUI WANG, HONGQIAO FAN, XIAOHUA PEI","doi":"10.32604/biocell.2023.030742","DOIUrl":"https://doi.org/10.32604/biocell.2023.030742","url":null,"abstract":"<b>Background:</b> The development and prognosis of breast cancer are intricately linked to psychological stress. In addition, depression is the most common psychological comorbidity among breast cancer survivors, and reportedly, Fang-Xia-Dihuang decoction (FXDH) can effectively manage depression in such patients. However, its pharmacological and molecular mechanisms remain obscure. <b>Methods:</b> Public databases were used for obtaining active components and related targets. Main active components were further verified by ultra-high-performance liquid chromatography-high-resolution mass spectrometry (UPLC-HRMS). Protein–protein interaction and enrichment analyses were taken to predict potential hub targets and related pathways. Molecule docking was used to understand the interactions between main compounds and hub targets. In addition, an animal model of breast cancer combined with depression was established to evaluate the intervention effect of FXDH and verify the pathways screened by network pharmacology. <b>Results:</b> 174 active components of FXDH and 163 intersection targets of FXDH, breast cancer, and depression were identified. Quercetin, methyl ferulate, luteolin, ferulaldehyde, wogonin, and diincarvilone were identified as the principal active components of FXDH. Protein–protein interaction and KEGG enrichment analyses revealed that the phosphoinositide-3-kinase–protein kinase B (PI3K/AKT) and Janus kinase/signal transducer and activator of transcription (JAK2/STAT3) signaling pathways played a crucial role in mediating the efficacy of FXDH for inhibiting breast cancer progression induced by depression. In addition, <i>in vivo</i> experiments revealed that FXDH ameliorated depression-like behavior in mice and inhibited excessive tumor growth in mice with breast cancer and depression. FXDH treatment downregulated the expression of epinephrine, PI3K, AKT, STAT3, and JAK2 compared with the control treatment (<i>p</i> < 0.05). Molecular docking verified the relationship between the six primary components of FXDH and the three most important targets, including phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha (PIK3CA), AKT, and STAT3. <b>Conclusion:</b> This study provides a scientific basis to support the clinical application of FXDH for improving depression-like behavior and inhibiting breast cancer progression promoted by chronic stress. The therapeutic effects FXDH may be closely related to the PI3K/AKT and JAK2/STAT3 pathways. This finding helps better understand the regulatory mechanisms underlying the efficacy of FXDH.","PeriodicalId":55384,"journal":{"name":"Biocell","volume":"88 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"135753664","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-01-01DOI: 10.32604/biocell.2023.029277
CHUNYANG XU, CAIYUN YANG, JINSONG ZHANG, XIAOHUA PAN, JUN WANG, LEI JIANG, HONGWEI YE, BO CHEN
Background: The lung is one of the primary target organs of hydrogen sulfide (H2S), as exposure to H2S can cause acute lung injury (ALI) and pulmonary edema. Dexamethasone (Dex) exerts a protective effect on ALI caused by exposure to toxic gases and is commonly used in the clinic; however, the underlying mechanisms remain elusive, and the dose is unclear. Methods:In vivo experiments: divided C57BL6 mice into 6 groups at random, 12 in each group. The mice were exposed to H2S for 3 h and 5 or 50 mg/kg Dex pretreated before exposure, sacrificed 12 h later. The morphological changes of HE staining and the ultrastructural changes of lungs under transmission electron microscopy were evaluated. The wet/dry ratio of lung tissue was measured. Bronchial alveolar lavage fluid (BALF) protein content and lung permeability index were detected. The expression of AQP5 protein was measured by immunohistochemistry and Western Blot (WB). In vitro experiments: divided human lung adenocarcinoma cell line A549 into 4 groups. 1 μmol/L dexamethasone was added to pre-incubation. The WB analyzed the protein of p-ERK1/2, p-JNK, and p-p38 in MAPK pathway after 1 h of NaHS exposure; six hours after NaHS exposure, the AQP5 protein was measured by WB. Results: Dex treatment could significantly attenuate the H2S-induced destruction to the alveolar wall, increase the wet-to-dry weight ratio and decrease pulmonary permeability index, with high-dose dexamethasone seemingly functioning better. Additionally, our previous studies showed that aquaporin 5 (AQP 5), a critical protein that regulates water flux, decreased both in a mouse and cell model following the exposure to H2S. This study indicates that tThe decrease in AQP 5 can be alleviated by Dex treatment. Additionally, the mitogen activated protein kinase (MAPK) pathway may be involved in the protective effects of Dex in ALI caused by exposure to H2S since H2S-induced MAPK activation could be inhibited by Dex. Conclusion: The present results indicate that AQP 5 may be considered a therapeutic target for Dex in H2S or other hazardous gases-induced ALI.
{"title":"The therapeutic mechanism of dexamethasone in lung injury induced by hydrogen sulfide","authors":"CHUNYANG XU, CAIYUN YANG, JINSONG ZHANG, XIAOHUA PAN, JUN WANG, LEI JIANG, HONGWEI YE, BO CHEN","doi":"10.32604/biocell.2023.029277","DOIUrl":"https://doi.org/10.32604/biocell.2023.029277","url":null,"abstract":"<b>Background:</b> The lung is one of the primary target organs of hydrogen sulfide (H<sub>2</sub>S), as exposure to H<sub>2</sub>S can cause acute lung injury (ALI) and pulmonary edema. Dexamethasone (Dex) exerts a protective effect on ALI caused by exposure to toxic gases and is commonly used in the clinic; however, the underlying mechanisms remain elusive, and the dose is unclear. <b>Methods:</b> <i>In vivo</i> experiments: divided C57BL6 mice into 6 groups at random, 12 in each group. The mice were exposed to H<sub>2</sub>S for 3 h and 5 or 50 mg/kg Dex pretreated before exposure, sacrificed 12 h later. The morphological changes of HE staining and the ultrastructural changes of lungs under transmission electron microscopy were evaluated. The wet/dry ratio of lung tissue was measured. Bronchial alveolar lavage fluid (BALF) protein content and lung permeability index were detected. The expression of AQP5 protein was measured by immunohistochemistry and Western Blot (WB). <i>In vitro</i> experiments: divided human lung adenocarcinoma cell line A549 into 4 groups. 1 μmol/L dexamethasone was added to pre-incubation. The WB analyzed the protein of p-ERK1/2, p-JNK, and p-p38 in MAPK pathway after 1 h of NaHS exposure; six hours after NaHS exposure, the AQP5 protein was measured by WB. <b>Results:</b> Dex treatment could significantly attenuate the H<sub>2</sub>S-induced destruction to the alveolar wall, increase the wet-to-dry weight ratio and decrease pulmonary permeability index, with high-dose dexamethasone seemingly functioning better. Additionally, our previous studies showed that aquaporin 5 (AQP 5), a critical protein that regulates water flux, decreased both in a mouse and cell model following the exposure to H<sub>2</sub>S. This study indicates that tThe decrease in AQP 5 can be alleviated by Dex treatment. Additionally, the mitogen activated protein kinase (MAPK) pathway may be involved in the protective effects of Dex in ALI caused by exposure to H<sub>2</sub>S since H<sub>2</sub>S-induced MAPK activation could be inhibited by Dex. <b>Conclusion:</b> The present results indicate that AQP 5 may be considered a therapeutic target for Dex in H<sub>2</sub>S or other hazardous gases-induced ALI.","PeriodicalId":55384,"journal":{"name":"Biocell","volume":"281 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"135755121","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-01-01DOI: 10.32604/biocell.2023.029986
GAOZHONG LI, FUXIN LI, NING WEI, QING JIA
Background: This study was aimed at identifying natural killer (NK) cell-related genes to design a risk prognosis model for the accurate evaluation of gastric cancer (GC) prognosis. Methods: We obtained NK cell-related genes from various databases, followed by Cox regression analysis and molecular typing to identify prognostic genes. Various immune algorithms and enrichment analyses were used to investigate the mutations, immune status, and pathway variations among different genotypes. The key prognostic genes were assessed using the least absolute shrinkage and selection operator (Lasso) regression analysis and univariate Cox regression analysis. Thereafter, the risk score (RS) prognosis model was constructed based on the selected important prognostic genes. A Receiver Operating Characteristics (ROC) curve was plotted for analyzing the robustness of the model. Subsequently, the decision and calibration curves were used for assessing the reliability and prediction accuracy of the proposed model. The ‘pRRophetic’ R software package was utilized for predicting the half-maximal inhibitory concentration (IC50) of immunotherapy and chemotherapy drugs. Results: We screened 21 prognostic genes and three molecular subtypes and found that the C1 subtype had the worst prognosis. Further, the pathways promoting tumor proliferation, such as epithelial-mesenchymal transition were significantly up-regulated. The results also showed that the macrophages in the M2 stage were significantly infiltrated in the C1 subtype, and there was significant overexpression in the C1 subtype, accompanied by a severe inflammatory reaction. The C1 was highly sensitive to drugs like 5-fluorouracil and paclitaxel. The ROC, calibration curve, and decision curve showed that the risk model was robust and strongly reliable. Conclusion: Overall, our proposed NK cell-related RS model can be used as a more accurate prediction index for GC patients, providing a valuable contribution to personalized medicine.
{"title":"Designing a risk prognosis model based on natural killer cell-linked genes to accurately evaluate the prognosis of gastric cancer","authors":"GAOZHONG LI, FUXIN LI, NING WEI, QING JIA","doi":"10.32604/biocell.2023.029986","DOIUrl":"https://doi.org/10.32604/biocell.2023.029986","url":null,"abstract":"<b>Background:</b> This study was aimed at identifying natural killer (NK) cell-related genes to design a risk prognosis model for the accurate evaluation of gastric cancer (GC) prognosis. <b>Methods:</b> We obtained NK cell-related genes from various databases, followed by Cox regression analysis and molecular typing to identify prognostic genes. Various immune algorithms and enrichment analyses were used to investigate the mutations, immune status, and pathway variations among different genotypes. The key prognostic genes were assessed using the least absolute shrinkage and selection operator (Lasso) regression analysis and univariate Cox regression analysis. Thereafter, the risk score (RS) prognosis model was constructed based on the selected important prognostic genes. A Receiver Operating Characteristics (ROC) curve was plotted for analyzing the robustness of the model. Subsequently, the decision and calibration curves were used for assessing the reliability and prediction accuracy of the proposed model. The ‘pRRophetic’ R software package was utilized for predicting the half-maximal inhibitory concentration (IC50) of immunotherapy and chemotherapy drugs. <b>Results:</b> We screened 21 prognostic genes and three molecular subtypes and found that the C1 subtype had the worst prognosis. Further, the pathways promoting tumor proliferation, such as epithelial-mesenchymal transition were significantly up-regulated. The results also showed that the macrophages in the M2 stage were significantly infiltrated in the C1 subtype, and there was significant overexpression in the C1 subtype, accompanied by a severe inflammatory reaction. The C1 was highly sensitive to drugs like 5-fluorouracil and paclitaxel. The ROC, calibration curve, and decision curve showed that the risk model was robust and strongly reliable. <b>Conclusion:</b> Overall, our proposed NK cell-related RS model can be used as a more accurate prediction index for GC patients, providing a valuable contribution to personalized medicine.","PeriodicalId":55384,"journal":{"name":"Biocell","volume":"28 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"135755386","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-01-01DOI: 10.32604/biocell.2023.024591
Wei Lu, Kan Guo, Dianmei Xi, Zhaoxia Xia
: Background: Mesenchymal stem cell (MSC)-derived exosomes are closely related to pyroptosis in diabetic nephropathy (DN). This study aimed to explore the protective effect of exosomal miR-30a-5p on podocyte pyroptosis in DN. Methods: Streptozotocin was used to establish the mouse model of DN. Human bone marrow MSC-derived exosomes were extracted and identi fi ed via transmission electron microscopy, nanoparticle tracking analysis, and western blotting. MiR-30a-5p mimics and non-control (NC) mimics were transfected into MSCs and podocytes, and exosomes were isolated from the MSCs. High glucose (HG)-induced podocyte model was established to determine the effect of exosomal miR-30a-5p on pyroptosis and in fl ammation in vitro . Results: MiR-30a-5p was expressed at low levels in DN models, while NLR family pyrin domain containing 3 (NLRP3), caspase-1, gasdermin-N (GSDMD-N), and pro-in fl ammatory factors (tumor necrosis factor-alpha, interleukin (IL)-1beta, and IL-18) were augmented. In vitro , miR-30a-5p expression in the HG-damaged podocytes was down-regulated, while NLRP3 was up-regulated. Interestingly, miR-30a-5p overexpression diminished HG-induced podocyte injury, as proven by increased activity and decreased pyroptosis of podocytes. Concurrently, the up-regulation of miR-30a-5p could inhibit the expression of pro-in fl ammatory factors, caspase-1, GSDMD-N, and NLRP3 in HG-induced podocytes. MSC-derived exosomal miR-30a-5p treatment of HG-damaged cells has similar effects to miR-30a-5p mimics treatment. Overexpression of NLRP3 reversed the effect of miR-30a-5p mimics on HG-induced podocytes. Conclusion: This research con fi rmed that exosomal miR-30a-5p regulates pyroptosis via mediating NLRP3 in DN.
{"title":"Exosomal miR-30a-5p targets NLRP3 to suppress podocyte pyroptosis in diabetic nephropathy","authors":"Wei Lu, Kan Guo, Dianmei Xi, Zhaoxia Xia","doi":"10.32604/biocell.2023.024591","DOIUrl":"https://doi.org/10.32604/biocell.2023.024591","url":null,"abstract":": Background: Mesenchymal stem cell (MSC)-derived exosomes are closely related to pyroptosis in diabetic nephropathy (DN). This study aimed to explore the protective effect of exosomal miR-30a-5p on podocyte pyroptosis in DN. Methods: Streptozotocin was used to establish the mouse model of DN. Human bone marrow MSC-derived exosomes were extracted and identi fi ed via transmission electron microscopy, nanoparticle tracking analysis, and western blotting. MiR-30a-5p mimics and non-control (NC) mimics were transfected into MSCs and podocytes, and exosomes were isolated from the MSCs. High glucose (HG)-induced podocyte model was established to determine the effect of exosomal miR-30a-5p on pyroptosis and in fl ammation in vitro . Results: MiR-30a-5p was expressed at low levels in DN models, while NLR family pyrin domain containing 3 (NLRP3), caspase-1, gasdermin-N (GSDMD-N), and pro-in fl ammatory factors (tumor necrosis factor-alpha, interleukin (IL)-1beta, and IL-18) were augmented. In vitro , miR-30a-5p expression in the HG-damaged podocytes was down-regulated, while NLRP3 was up-regulated. Interestingly, miR-30a-5p overexpression diminished HG-induced podocyte injury, as proven by increased activity and decreased pyroptosis of podocytes. Concurrently, the up-regulation of miR-30a-5p could inhibit the expression of pro-in fl ammatory factors, caspase-1, GSDMD-N, and NLRP3 in HG-induced podocytes. MSC-derived exosomal miR-30a-5p treatment of HG-damaged cells has similar effects to miR-30a-5p mimics treatment. Overexpression of NLRP3 reversed the effect of miR-30a-5p mimics on HG-induced podocytes. Conclusion: This research con fi rmed that exosomal miR-30a-5p regulates pyroptosis via mediating NLRP3 in DN.","PeriodicalId":55384,"journal":{"name":"Biocell","volume":"36 1","pages":""},"PeriodicalIF":1.2,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"73838290","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-01-01DOI: 10.32604/biocell.2023.029493
Jing Jin, Xie Li, Ting Qiu, Lei Song, Yuanyue Cui, Guangya Zhang, Shu Li, Wencheng Zhao
{"title":"Expression profiles of circulating tRNA-derived small RNAs and their potential role in diabetes","authors":"Jing Jin, Xie Li, Ting Qiu, Lei Song, Yuanyue Cui, Guangya Zhang, Shu Li, Wencheng Zhao","doi":"10.32604/biocell.2023.029493","DOIUrl":"https://doi.org/10.32604/biocell.2023.029493","url":null,"abstract":"","PeriodicalId":55384,"journal":{"name":"Biocell","volume":"51 1","pages":""},"PeriodicalIF":1.2,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"80257166","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-01-01DOI: 10.32604/biocell.2023.026148
Jia Liu, Faping Wang, Bo Yuan, F. Luo
{"title":"Transcriptional factor RUNX1: A potential therapeutic target for fibrotic pulmonary disease","authors":"Jia Liu, Faping Wang, Bo Yuan, F. Luo","doi":"10.32604/biocell.2023.026148","DOIUrl":"https://doi.org/10.32604/biocell.2023.026148","url":null,"abstract":"","PeriodicalId":55384,"journal":{"name":"Biocell","volume":"38 1","pages":""},"PeriodicalIF":1.2,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"78381608","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-01-01DOI: 10.32604/biocell.2023.025154
Miaomiao Li, Danyang Chen, Junyi Ke, Ruilin Zheng, Jingyao Su, Z. Zheng, Jieyi Luo, Hanran Mai, Fan Jiang, Yan-xia Qu, Xiaoqiong Gu, B. Zhu, Yinghua Li, Liandong Zuo
A H2O2-induced oxidative stress injury cell model was established to investigate the antioxidant effect of nanoselenium on mouse spermatocyte lines and the regulation mechanism of the expression level and activity of seleniumcontaining antioxidant enzymes induced by oxidative stress. A safe and effective nano-drug system of functionalized selenium-containing nanoparticles (SeNPs) was developed with lentinan (LNT) (SeNPs@LNT). Mice spermatocyte line GC2-spg cells were treated with SeNPs@LNT (1, 2, 4, 8, 16, 32 μM) for 24–72 h to evaluate the cytotoxicity of selenium. GC2-spg cells were randomly divided into the following groups: control, hydrogen peroxide (H2O2), SeNPs@LNT, and H2O2+SeNPs@LNT groups. H2O2+SeNPs@LNT group was pretreated with SeNPs@LNT 4 μM for 12 h, followed by H2O2 600 μM for 8 h. The cell viability decreased in the H2O2 group and increased significantly in the SeNPs@LNT group. Compared with the H2O2 group, the SeNPs@LNT+H2O2 group exhibited obvious red fluorescence, indicating a higher level of mitochondrial membrane potential. The content of intracellular reactive oxygen species (ROS) in the SeNPs@LNT group reduced significantly, and the intensity of green fluorescence in the SeNPs@LNT+H2O2 group decreased significantly compared with the H2O2 group, indicating the inhibitory effect of SeNPs@LNT on the generation of ROS-induced oxidative stress. The activity of GPx and SOD increased significantly in the SeNPs@LNT group. The expression of p53 decreased significantly under the intervention of nano-selenium, and GPx1 expression increased. In the oxidative stress group, the expressions of DNA damage-related proteins and apoptosis-related proteins were higher than those in other groups. Thus, SeNPs@LNT can promote GC2-spg cell proliferation, improve GPx and SOD activities, remove intracellular ROS, and reduce mitochondrial damage and functional abnormalities caused by oxidative stress by regulating the ERK and p53 protein levels. SeNPs@LNT has good biological activity and antioxidant effect, which can be used to protect the male reproductive system from
{"title":"Inhibition of H2O2-induced apoptosis of GC2-spg cells by functionalized selenium nanoparticles with lentinan through ROS-mediated ERK/p53 signaling pathways","authors":"Miaomiao Li, Danyang Chen, Junyi Ke, Ruilin Zheng, Jingyao Su, Z. Zheng, Jieyi Luo, Hanran Mai, Fan Jiang, Yan-xia Qu, Xiaoqiong Gu, B. Zhu, Yinghua Li, Liandong Zuo","doi":"10.32604/biocell.2023.025154","DOIUrl":"https://doi.org/10.32604/biocell.2023.025154","url":null,"abstract":"A H2O2-induced oxidative stress injury cell model was established to investigate the antioxidant effect of nanoselenium on mouse spermatocyte lines and the regulation mechanism of the expression level and activity of seleniumcontaining antioxidant enzymes induced by oxidative stress. A safe and effective nano-drug system of functionalized selenium-containing nanoparticles (SeNPs) was developed with lentinan (LNT) (SeNPs@LNT). Mice spermatocyte line GC2-spg cells were treated with SeNPs@LNT (1, 2, 4, 8, 16, 32 μM) for 24–72 h to evaluate the cytotoxicity of selenium. GC2-spg cells were randomly divided into the following groups: control, hydrogen peroxide (H2O2), SeNPs@LNT, and H2O2+SeNPs@LNT groups. H2O2+SeNPs@LNT group was pretreated with SeNPs@LNT 4 μM for 12 h, followed by H2O2 600 μM for 8 h. The cell viability decreased in the H2O2 group and increased significantly in the SeNPs@LNT group. Compared with the H2O2 group, the SeNPs@LNT+H2O2 group exhibited obvious red fluorescence, indicating a higher level of mitochondrial membrane potential. The content of intracellular reactive oxygen species (ROS) in the SeNPs@LNT group reduced significantly, and the intensity of green fluorescence in the SeNPs@LNT+H2O2 group decreased significantly compared with the H2O2 group, indicating the inhibitory effect of SeNPs@LNT on the generation of ROS-induced oxidative stress. The activity of GPx and SOD increased significantly in the SeNPs@LNT group. The expression of p53 decreased significantly under the intervention of nano-selenium, and GPx1 expression increased. In the oxidative stress group, the expressions of DNA damage-related proteins and apoptosis-related proteins were higher than those in other groups. Thus, SeNPs@LNT can promote GC2-spg cell proliferation, improve GPx and SOD activities, remove intracellular ROS, and reduce mitochondrial damage and functional abnormalities caused by oxidative stress by regulating the ERK and p53 protein levels. SeNPs@LNT has good biological activity and antioxidant effect, which can be used to protect the male reproductive system from","PeriodicalId":55384,"journal":{"name":"Biocell","volume":"333 1","pages":""},"PeriodicalIF":1.2,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"77390487","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-01-01DOI: 10.32604/biocell.2023.025157
Xianglai Jiang, Jin He, Yongfeng Wang, Jiahui Liu, Xiangyang Li, Xiaoniu He, Hui Cai
B and T-lymphocyte attenuator (BTLA) plays an immunosuppressive role by inhibiting Tand B-cell functions. BTLA is associated with a variety of diseases, especially cancer immunity. However, the function of BTLA in various cancers and its clinical prognostic value have still not been comprehensively analyzed. This study aimed to identify the relationship between BTLA and cancer from the perspectives of differences in BTLA expression, its clinical value, immune infiltration, and the correlation with immune-related genes in various cancers. Data regarding mRNA expression, miRNA expression, lncRNA expression, and clinical data of patients of 33 existing cancers were collected from the TCGA database. Target miRNA of BTLA and the lncRNA that interacts with the target miRNA were obtained from the StarBase database. Based on bioinformatics analysis methods, the relationship between various types of cancers and BTLA was thoroughly investigated, and a competing endogenous RNA network of BTLA, target miRNA, and interacting lncRNA was constructed. The Kaplan-Meier (KM) prognostic analysis of BTLA and target miRNA (has-miR-137) in various types of cancers was completed using the KM plotter. BTLA expression varied in different cancers, with statistical significance in nine cancer types. KM plotter to analyze the overall survival (OS) and regression-free survival prognosis of cancer patients revealed that the BTLA expression was statistically different in the OS of 11 types of cancers out of 21 types of cancers; the OS of 8 type of cancers was also statistically different. Correlation analysis of tumor immune genes revealed a positive correlation of BTLA expression with immunosuppressive gene (CTLA4 and PDCD1) expression. Gene Set Enrichment Analysis showed that BTLA and its co-expressed genes mainly act through biological processes and pathways, including immune response regulation, cell surface receptor signaling pathway, antigen binding, antigen receptor-mediated signaling pathway, and leukocyte migration. BTLA has the potential as a prognostic marker for CLL, COAD, NSCLC, and OV and a diagnostic marker for CLL, COAD, and KIRC. BTLA has a close and complex relationship with the occurrence and development of tumors, and cancer immunotherapy for BTLA is worthy of further analysis.
{"title":"A pan-cancer analysis of the biological function and clinical value of BTLA in tumors","authors":"Xianglai Jiang, Jin He, Yongfeng Wang, Jiahui Liu, Xiangyang Li, Xiaoniu He, Hui Cai","doi":"10.32604/biocell.2023.025157","DOIUrl":"https://doi.org/10.32604/biocell.2023.025157","url":null,"abstract":"B and T-lymphocyte attenuator (BTLA) plays an immunosuppressive role by inhibiting Tand B-cell functions. BTLA is associated with a variety of diseases, especially cancer immunity. However, the function of BTLA in various cancers and its clinical prognostic value have still not been comprehensively analyzed. This study aimed to identify the relationship between BTLA and cancer from the perspectives of differences in BTLA expression, its clinical value, immune infiltration, and the correlation with immune-related genes in various cancers. Data regarding mRNA expression, miRNA expression, lncRNA expression, and clinical data of patients of 33 existing cancers were collected from the TCGA database. Target miRNA of BTLA and the lncRNA that interacts with the target miRNA were obtained from the StarBase database. Based on bioinformatics analysis methods, the relationship between various types of cancers and BTLA was thoroughly investigated, and a competing endogenous RNA network of BTLA, target miRNA, and interacting lncRNA was constructed. The Kaplan-Meier (KM) prognostic analysis of BTLA and target miRNA (has-miR-137) in various types of cancers was completed using the KM plotter. BTLA expression varied in different cancers, with statistical significance in nine cancer types. KM plotter to analyze the overall survival (OS) and regression-free survival prognosis of cancer patients revealed that the BTLA expression was statistically different in the OS of 11 types of cancers out of 21 types of cancers; the OS of 8 type of cancers was also statistically different. Correlation analysis of tumor immune genes revealed a positive correlation of BTLA expression with immunosuppressive gene (CTLA4 and PDCD1) expression. Gene Set Enrichment Analysis showed that BTLA and its co-expressed genes mainly act through biological processes and pathways, including immune response regulation, cell surface receptor signaling pathway, antigen binding, antigen receptor-mediated signaling pathway, and leukocyte migration. BTLA has the potential as a prognostic marker for CLL, COAD, NSCLC, and OV and a diagnostic marker for CLL, COAD, and KIRC. BTLA has a close and complex relationship with the occurrence and development of tumors, and cancer immunotherapy for BTLA is worthy of further analysis.","PeriodicalId":55384,"journal":{"name":"Biocell","volume":"246 1","pages":""},"PeriodicalIF":1.2,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"76755198","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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