Mei-Ling Wang, Rui Liu, Li-Mei Zhang, Bin Zhao, Rui Jia, Yang Zhao, Ya-Lin Xi, Jing-Xia Ma, He Ma
Purpose: We report two cases diagnosed as acute necrotizing encephalopathy (ANE) with acute onset and various clinical manifestations.
Methods: The patients' data were obtained from the medical records of the Binzhou Medical University Hospital in Binzhou, China. The clinical symptoms, laboratory examination, neuroimaging, treatment, and prognosis of the 2 patients were collected and analyzed.
Results: We report 2 adult ANE patients with acute onset. The first symptom was fever, followed by symptoms and signs of damage to the central nervous system. The patients were infected with herpes simplex virus and influenza virus, respectively. The main manifestation on brain magnetic resonance imaging was a mixed-signal of a "three-layer structure" in the bilateral thalamus. The first patient died. Based on the experience of the diagnosis and treatment of the first patient, combined with a review of the literature, the second patient was immediately treated with glucocorticoid pulse therapy combined with gamma globulin injection. This patient's condition was controlled, and the prognosis was good.
Conclusions: This study describes the clinical symptoms, laboratory examination, neuroimaging evidence, and treatment experience of ANE in adults. We believe that the progress of the disease may be controlled, and the prognosis may be improved if glucocorticoid pulse therapy combined with gamma globulin injection is used as soon as possible.
{"title":"Clinical Experience in the Diagnosis and Treatment of Adult Acute Necrotizing Encephalopathy.","authors":"Mei-Ling Wang, Rui Liu, Li-Mei Zhang, Bin Zhao, Rui Jia, Yang Zhao, Ya-Lin Xi, Jing-Xia Ma, He Ma","doi":"10.1159/000524955","DOIUrl":"https://doi.org/10.1159/000524955","url":null,"abstract":"<p><strong>Purpose: </strong>We report two cases diagnosed as acute necrotizing encephalopathy (ANE) with acute onset and various clinical manifestations.</p><p><strong>Methods: </strong>The patients' data were obtained from the medical records of the Binzhou Medical University Hospital in Binzhou, China. The clinical symptoms, laboratory examination, neuroimaging, treatment, and prognosis of the 2 patients were collected and analyzed.</p><p><strong>Results: </strong>We report 2 adult ANE patients with acute onset. The first symptom was fever, followed by symptoms and signs of damage to the central nervous system. The patients were infected with herpes simplex virus and influenza virus, respectively. The main manifestation on brain magnetic resonance imaging was a mixed-signal of a \"three-layer structure\" in the bilateral thalamus. The first patient died. Based on the experience of the diagnosis and treatment of the first patient, combined with a review of the literature, the second patient was immediately treated with glucocorticoid pulse therapy combined with gamma globulin injection. This patient's condition was controlled, and the prognosis was good.</p><p><strong>Conclusions: </strong>This study describes the clinical symptoms, laboratory examination, neuroimaging evidence, and treatment experience of ANE in adults. We believe that the progress of the disease may be controlled, and the prognosis may be improved if glucocorticoid pulse therapy combined with gamma globulin injection is used as soon as possible.</p>","PeriodicalId":19133,"journal":{"name":"Neuroimmunomodulation","volume":null,"pages":null},"PeriodicalIF":2.4,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10743757","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Qian Yu, Guangyao Li, Jiangjing Li, Li Sun, Yonghui Yang, Lei Tao
Background: Ischemic stroke is a major health issue that causes high incidents of morbidity and mortality worldwide. Irisin is an excise-induced protein that has exhibited pleiotropic properties. Accumulating evidence reveals its critical roles in the regulation of various cellular functions, including nervous system functions. This study aims to disclose the effect of irisin on rat cerebral neurons suffering from hypoxia/reoxygenation (H/R) treatment and to explore the potential underlying molecular mechanisms.
Methods: The percentage of rat cerebral neuron cell death was determined by flow cytometry analysis and MTT assay. The expression levels of target genes were measured by western blotting and real-time quantitative reverse transcription PCR assay.
Results: Our results demonstrated that irisin treatment substantially reduced H/R-induced apoptosis of rat cerebral neurons. Further investigation revealed that irisin treatment markedly decreased mitogen-activated protein kinase (MAPK) signaling pathway activation and suppressed pro-informatory cytokine expression in cerebral neurons with H/R challenge. Finally, we showed that the neuroprotective effect and anti-inflammatory effect of irisin were comparable with three MAPK signaling inhibitors.
Conclusion: Irisin exerts profound neuroprotective and anti-inflammatory effects on H/R-stimulated cerebral neurons by inhibiting the MAPK signaling activation. Therefore, irisin may serve as a potential drug for the treatment of patients with ischemic stroke.
{"title":"Irisin Protects Cerebral Neurons from Hypoxia/Reoxygenation via Suppression of Apoptosis and Expression of Pro-Inflammatory Cytokines.","authors":"Qian Yu, Guangyao Li, Jiangjing Li, Li Sun, Yonghui Yang, Lei Tao","doi":"10.1159/000524273","DOIUrl":"https://doi.org/10.1159/000524273","url":null,"abstract":"<p><strong>Background: </strong>Ischemic stroke is a major health issue that causes high incidents of morbidity and mortality worldwide. Irisin is an excise-induced protein that has exhibited pleiotropic properties. Accumulating evidence reveals its critical roles in the regulation of various cellular functions, including nervous system functions. This study aims to disclose the effect of irisin on rat cerebral neurons suffering from hypoxia/reoxygenation (H/R) treatment and to explore the potential underlying molecular mechanisms.</p><p><strong>Methods: </strong>The percentage of rat cerebral neuron cell death was determined by flow cytometry analysis and MTT assay. The expression levels of target genes were measured by western blotting and real-time quantitative reverse transcription PCR assay.</p><p><strong>Results: </strong>Our results demonstrated that irisin treatment substantially reduced H/R-induced apoptosis of rat cerebral neurons. Further investigation revealed that irisin treatment markedly decreased mitogen-activated protein kinase (MAPK) signaling pathway activation and suppressed pro-informatory cytokine expression in cerebral neurons with H/R challenge. Finally, we showed that the neuroprotective effect and anti-inflammatory effect of irisin were comparable with three MAPK signaling inhibitors.</p><p><strong>Conclusion: </strong>Irisin exerts profound neuroprotective and anti-inflammatory effects on H/R-stimulated cerebral neurons by inhibiting the MAPK signaling activation. Therefore, irisin may serve as a potential drug for the treatment of patients with ischemic stroke.</p>","PeriodicalId":19133,"journal":{"name":"Neuroimmunomodulation","volume":null,"pages":null},"PeriodicalIF":2.4,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10485169","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Elisabeth Veiz, Susann-Kristin Kieslich, Dirk Czesnik, Christoph Herrmann-Lingen, Thomas Meyer, Julia Staab
Objective: The vagus nerve constitutes the main component of the parasympathetic nervous system and plays an important role in the regulation of neuro-immune responses. Invasive stimulation of the vagus nerve produces anti-inflammatory effects; however, data on humoral immune responses of transcutaneous vagus nerve stimulation (tVNS) are rare. Therefore, the present study investigated changes in serum cytokine concentrations of interleukin-1β (IL-1β), IL-6, IL-8, and tumor necrosis factor α (TNFα) following a short-term, non-invasive stimulation of the vagus nerve.
Methods: Whole blood samples were collected before and after a short-lived application of active tVNS at the inner tragus as well as sham stimulation of the earlobe. Cytokine serum concentrations were determined in two healthy cohorts of younger (n = 20) and older participants (n = 19). Differences between active and sham conditions were analyzed using linear mixed models and post hoc F tests after applying Yeo-Johnson power transformations. This trial was part of a larger study registered on ClinicalTrials.gov (NCT05007743).
Results: In the young cohort, IL-6 and IL-1β concentrations were significantly increased after active stimulation, whereas they were slightly decreased after sham stimulation (IL-6: p = 0.012; IL-1β: p = 0.012). Likewise, in the older cohort, IL-1β and IL-8 concentrations were significantly elevated after active stimulation and reduced after sham application (IL-8: p = 0.007; IL-1β: p = 0.001). In contrast, circulating TNFα concentrations did not change significantly in either group.
Conclusion: Our results show that active tVNS led to an immediate increase in the serum concentrations of certain pro-inflammatory cytokines such as IL-1β, IL-6, and/or IL-8 in two independent cohorts of healthy study participants.
目的:迷走神经是副交感神经系统的主要组成部分,在神经免疫反应的调节中起重要作用。侵袭性刺激迷走神经产生抗炎作用;然而,关于经皮迷走神经刺激(tVNS)的体液免疫反应的数据很少。因此,本研究研究了短期、非侵入性刺激迷走神经后血清白细胞介素-1β (IL-1β)、IL-6、IL-8和肿瘤坏死因子α (TNFα)浓度的变化。方法:在短时间内内耳屏应用主动tVNS和假性耳垂刺激前后采集全血样本。在年轻(n = 20)和老年参与者(n = 19)两个健康队列中测定细胞因子血清浓度。采用线性混合模型和事后F检验分析了应用杨-约翰逊功率变换后主动和虚假条件之间的差异。该试验是ClinicalTrials.gov (NCT05007743)上注册的一项大型研究的一部分。结果:在年轻队列中,主动刺激后IL-6和IL-1β浓度显著升高,而假性刺激后IL-6和IL-1β浓度略有降低(IL-6: p = 0.012;IL-1β: p = 0.012)。同样,在老年队列中,主动刺激后IL-1β和IL-8浓度显著升高,假性刺激后IL-8浓度降低(IL-8: p = 0.007;IL-1β: p = 0.001)。相比之下,两组循环TNFα浓度均无显著变化。结论:我们的研究结果表明,在两个独立的健康研究参与者中,活跃的tVNS导致某些促炎细胞因子(如IL-1β、IL-6和/或IL-8)的血清浓度立即增加。
{"title":"Increased Concentrations of Circulating Interleukins following Non-Invasive Vagus Nerve Stimulation: Results from a Randomized, Sham-Controlled, Crossover Study in Healthy Subjects.","authors":"Elisabeth Veiz, Susann-Kristin Kieslich, Dirk Czesnik, Christoph Herrmann-Lingen, Thomas Meyer, Julia Staab","doi":"10.1159/000524646","DOIUrl":"https://doi.org/10.1159/000524646","url":null,"abstract":"<p><strong>Objective: </strong>The vagus nerve constitutes the main component of the parasympathetic nervous system and plays an important role in the regulation of neuro-immune responses. Invasive stimulation of the vagus nerve produces anti-inflammatory effects; however, data on humoral immune responses of transcutaneous vagus nerve stimulation (tVNS) are rare. Therefore, the present study investigated changes in serum cytokine concentrations of interleukin-1β (IL-1β), IL-6, IL-8, and tumor necrosis factor α (TNFα) following a short-term, non-invasive stimulation of the vagus nerve.</p><p><strong>Methods: </strong>Whole blood samples were collected before and after a short-lived application of active tVNS at the inner tragus as well as sham stimulation of the earlobe. Cytokine serum concentrations were determined in two healthy cohorts of younger (n = 20) and older participants (n = 19). Differences between active and sham conditions were analyzed using linear mixed models and post hoc F tests after applying Yeo-Johnson power transformations. This trial was part of a larger study registered on ClinicalTrials.gov (NCT05007743).</p><p><strong>Results: </strong>In the young cohort, IL-6 and IL-1β concentrations were significantly increased after active stimulation, whereas they were slightly decreased after sham stimulation (IL-6: p = 0.012; IL-1β: p = 0.012). Likewise, in the older cohort, IL-1β and IL-8 concentrations were significantly elevated after active stimulation and reduced after sham application (IL-8: p = 0.007; IL-1β: p = 0.001). In contrast, circulating TNFα concentrations did not change significantly in either group.</p><p><strong>Conclusion: </strong>Our results show that active tVNS led to an immediate increase in the serum concentrations of certain pro-inflammatory cytokines such as IL-1β, IL-6, and/or IL-8 in two independent cohorts of healthy study participants.</p>","PeriodicalId":19133,"journal":{"name":"Neuroimmunomodulation","volume":null,"pages":null},"PeriodicalIF":2.4,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10393167","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Introduction: Physical exercise is an important component of managing Alzheimer's disease (AD). miRNAs can be modulated by exercise intervention.
Objective: The study explored the involvement and potential mechanism of miR-192-5p in the protective effect of physical exercise on AD.
Methods: Ninety AD patients were enrolled, in which 45 cases accepted cycling training for continuous 3 months. The expression changes of miR-192-5p before and after exercise were analyzed by reverse transcription-quantitative PCR. 8-month-old APP/PS1 double Tg mice were used as the AD animal model. Mice in the voluntary exercise (VE) group received VE for 4 weeks. Morris water maze (MWM) test was used to evaluate the learning and memory function. Enzyme-linked immunosorbent assay was used to calculate the level of IL-1β, IL-6, and TNF-α.
Results: AD patients showed elevated MMSE scores, decreased ADAS-cog and NPI-Q scores after 3 months of exercise. miR-192-5p was downregulated in the serum of AD patients and correlated with the levels of MMSE score, ADAS-cog, and NPI-Q score. A positive association was detected between serum miR-192-5p with TNF-α, IL-6, and IL-1β levels. MiR-192-5p is downregulated in the hippocampus tissues of mice after VE. Overexpression of miR-192-5p reversed the neuroprotective effect of exercise on AD in mice and promoted the inflammatory response of AD mice.
Conclusion: MiR-192-5p can be modulated by the exercise intervention and involved in the protective effect of exercise on AD.
体育锻炼是控制阿尔茨海默病(AD)的重要组成部分。mirna可以通过运动干预来调节。目的:探讨miR-192-5p在体育锻炼对AD的保护作用中的作用及其潜在机制。方法:入选90例AD患者,其中45例接受连续3个月的自行车训练。采用逆转录-定量PCR分析运动前后miR-192-5p的表达变化。采用8月龄APP/PS1双Tg小鼠作为AD动物模型。自愿运动(VE)组小鼠连续4周接受VE治疗。Morris水迷宫(Morris water maze, MWM)测试大鼠的学习记忆功能。采用酶联免疫吸附法计算IL-1β、IL-6、TNF-α水平。结果:运动3个月后,AD患者MMSE评分升高,ADAS-cog和NPI-Q评分降低。AD患者血清中miR-192-5p水平下调,与MMSE评分、ADAS-cog、NPI-Q评分水平相关。血清miR-192-5p与TNF-α、IL-6和IL-1β水平呈正相关。VE后小鼠海马组织中MiR-192-5p表达下调。miR-192-5p的过表达逆转了运动对小鼠AD的神经保护作用,促进了AD小鼠的炎症反应。结论:MiR-192-5p可通过运动干预调节,参与运动对AD的保护作用。
{"title":"Exercise-Mediated Alteration of miR-192-5p Is Associated with Cognitive Improvement in Alzheimer's Disease.","authors":"Zhaomei Qin, Xingjun Han, Jing Ran, Shanshan Guo, Lina Lv","doi":"10.1159/000516928","DOIUrl":"https://doi.org/10.1159/000516928","url":null,"abstract":"<p><strong>Introduction: </strong>Physical exercise is an important component of managing Alzheimer's disease (AD). miRNAs can be modulated by exercise intervention.</p><p><strong>Objective: </strong>The study explored the involvement and potential mechanism of miR-192-5p in the protective effect of physical exercise on AD.</p><p><strong>Methods: </strong>Ninety AD patients were enrolled, in which 45 cases accepted cycling training for continuous 3 months. The expression changes of miR-192-5p before and after exercise were analyzed by reverse transcription-quantitative PCR. 8-month-old APP/PS1 double Tg mice were used as the AD animal model. Mice in the voluntary exercise (VE) group received VE for 4 weeks. Morris water maze (MWM) test was used to evaluate the learning and memory function. Enzyme-linked immunosorbent assay was used to calculate the level of IL-1β, IL-6, and TNF-α.</p><p><strong>Results: </strong>AD patients showed elevated MMSE scores, decreased ADAS-cog and NPI-Q scores after 3 months of exercise. miR-192-5p was downregulated in the serum of AD patients and correlated with the levels of MMSE score, ADAS-cog, and NPI-Q score. A positive association was detected between serum miR-192-5p with TNF-α, IL-6, and IL-1β levels. MiR-192-5p is downregulated in the hippocampus tissues of mice after VE. Overexpression of miR-192-5p reversed the neuroprotective effect of exercise on AD in mice and promoted the inflammatory response of AD mice.</p><p><strong>Conclusion: </strong>MiR-192-5p can be modulated by the exercise intervention and involved in the protective effect of exercise on AD.</p>","PeriodicalId":19133,"journal":{"name":"Neuroimmunomodulation","volume":null,"pages":null},"PeriodicalIF":2.4,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39179663","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Introduction: Thyroid-stimulating hormone receptor (TSHR) is widely expressed in human tissues and cells. TSHR is not only involved in thyroid disease but also in the neuroendocrine-immune regulatory network. However, no study has exclusively focused on the expression and function of TSHR in natural killer (NK) cells.
Methods: We studied TSHR expression using reverse transcription PCR to verify TSHR mRNA transcripts in human and mouse NK cells. Human and mouse thyroid and liver tissues as well as peripheral blood mononuclear cells (PBMCs) or spleen lymphoid cells (SLCs) were used as controls. The TSHR protein levels in NK-92 cells were determined by immunofluorescence staining. The function of TSHR in NK cells was investigated by measuring the TSH-stimulated cAMP levels.
Results: TSHR mRNA was detected in human and mouse NK cells as well as in NK-92 cells and had the same sequence as that of thyroid-derived, PBMC-derived, and liver-derived mRNA. The TSHR protein was also expressed in the cell membrane of NK-92 cells. Furthermore, the cAMP levels in NK-92 cells were significantly higher after adding 102 mIU/mL of bovine TSH at p < 0.05, which stimulated cAMP production in NK-92 cells.
Conclusions: Our findings confirm that TSHR is present and functional in NK cells and provide key clues for the potential regulatory effects of TSH on TSHR in NK cells in the immune system.
{"title":"Presence of TSHR in NK Cells and Action of TSH on NK Cells.","authors":"Qingqing Yang, Jingyi Li, Chunjia Kou, Li Zhang, Xiansheng Wang, Yu Long, Jiajia Ni, Shuqi Li, Haiqing Zhang","doi":"10.1159/000516925","DOIUrl":"https://doi.org/10.1159/000516925","url":null,"abstract":"<p><strong>Introduction: </strong>Thyroid-stimulating hormone receptor (TSHR) is widely expressed in human tissues and cells. TSHR is not only involved in thyroid disease but also in the neuroendocrine-immune regulatory network. However, no study has exclusively focused on the expression and function of TSHR in natural killer (NK) cells.</p><p><strong>Methods: </strong>We studied TSHR expression using reverse transcription PCR to verify TSHR mRNA transcripts in human and mouse NK cells. Human and mouse thyroid and liver tissues as well as peripheral blood mononuclear cells (PBMCs) or spleen lymphoid cells (SLCs) were used as controls. The TSHR protein levels in NK-92 cells were determined by immunofluorescence staining. The function of TSHR in NK cells was investigated by measuring the TSH-stimulated cAMP levels.</p><p><strong>Results: </strong>TSHR mRNA was detected in human and mouse NK cells as well as in NK-92 cells and had the same sequence as that of thyroid-derived, PBMC-derived, and liver-derived mRNA. The TSHR protein was also expressed in the cell membrane of NK-92 cells. Furthermore, the cAMP levels in NK-92 cells were significantly higher after adding 102 mIU/mL of bovine TSH at p < 0.05, which stimulated cAMP production in NK-92 cells.</p><p><strong>Conclusions: </strong>Our findings confirm that TSHR is present and functional in NK cells and provide key clues for the potential regulatory effects of TSH on TSHR in NK cells in the immune system.</p>","PeriodicalId":19133,"journal":{"name":"Neuroimmunomodulation","volume":null,"pages":null},"PeriodicalIF":2.4,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39322492","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2022-01-01Epub Date: 2021-08-24DOI: 10.1159/000518215
Meijing Wang, Hongyan Liu, Lufeng Xu, Mengmeng Li, Ming Zhao
Introduction: Isoflurane inhalation leads to apoptotic neurodegeneration and further results in learning and cognitive dysfunction. Notoginsenoside R1 (NGR1), a major ingredient from Radix notoginseng, has been reported to exert neuroprotective effect during brain or neuron injury. This study aimed to investigate the effect of NGR1 on neurological impairment.
Methods: Sixty-four male Sprague Dawley rat pups (15-20 g) of postnatal day 7 were recruited. Spatial learning and memory were assessed by the Morris water maze test, and the neurological severity score was determined. Real-time quantitative PCR was used to detect the expression levels of microRNA (miR)-29a. Enzyme-linked immunosorbent assay was applied to estimate the levels of interleukin-1β (IL-1β), interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α) in the hippocampal tissues.
Results: NGR1 attenuated neurological impairment induced by isoflurane, shown by the decrease in neurological function score and escape latency and the increase in staying time in the original quadrant in rats. NGR1 reversed the downregulation of miR-29a expression induced by isoflurane treatment. After the treatment of NGR1, the elevated levels of IL-6, TNF-α, and IL-1β induced by isoflurane were all decreased significantly in the hippocampal tissues of rats. Additionally, the repressive action of NGR1 in neurological impairment and neuroinflammation was eliminated by downregulating miR-29a in rats.
Conclusion: NGR1 protects against isoflurane-induced neurological impairment. The protective effect of NGR1 might be achieved by promoting the expression of miR-29a and preventing inflammatory response.
{"title":"The Protective Effect of Notoginsenoside R1 on Isoflurane-Induced Neurological Impairment in the Rats via Regulating miR-29a Expression and Neuroinflammation.","authors":"Meijing Wang, Hongyan Liu, Lufeng Xu, Mengmeng Li, Ming Zhao","doi":"10.1159/000518215","DOIUrl":"https://doi.org/10.1159/000518215","url":null,"abstract":"<p><strong>Introduction: </strong>Isoflurane inhalation leads to apoptotic neurodegeneration and further results in learning and cognitive dysfunction. Notoginsenoside R1 (NGR1), a major ingredient from Radix notoginseng, has been reported to exert neuroprotective effect during brain or neuron injury. This study aimed to investigate the effect of NGR1 on neurological impairment.</p><p><strong>Methods: </strong>Sixty-four male Sprague Dawley rat pups (15-20 g) of postnatal day 7 were recruited. Spatial learning and memory were assessed by the Morris water maze test, and the neurological severity score was determined. Real-time quantitative PCR was used to detect the expression levels of microRNA (miR)-29a. Enzyme-linked immunosorbent assay was applied to estimate the levels of interleukin-1β (IL-1β), interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α) in the hippocampal tissues.</p><p><strong>Results: </strong>NGR1 attenuated neurological impairment induced by isoflurane, shown by the decrease in neurological function score and escape latency and the increase in staying time in the original quadrant in rats. NGR1 reversed the downregulation of miR-29a expression induced by isoflurane treatment. After the treatment of NGR1, the elevated levels of IL-6, TNF-α, and IL-1β induced by isoflurane were all decreased significantly in the hippocampal tissues of rats. Additionally, the repressive action of NGR1 in neurological impairment and neuroinflammation was eliminated by downregulating miR-29a in rats.</p><p><strong>Conclusion: </strong>NGR1 protects against isoflurane-induced neurological impairment. The protective effect of NGR1 might be achieved by promoting the expression of miR-29a and preventing inflammatory response.</p>","PeriodicalId":19133,"journal":{"name":"Neuroimmunomodulation","volume":null,"pages":null},"PeriodicalIF":2.4,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39410771","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Introduction: Neuropathic pain (NP) is one of the most severe chronic pain types. In recent years, more and more studies have shown that long noncoding RNA (LncRNA) plays a key role in a variety of human diseases, including NP. However, the role of LncRNA prostate cancer-associated transcript 19 (PCAT19) in NP and its specific mechanism remain unclear.
Methods: A chronic constrictive injury (CCI) rat model was established. Rat paw withdrawal threshold and paw withdrawal latency were used to evaluate the neuronal pain behavior of rats in this model. mRNA expression of PCAT19, neuroinflammatory factor, microRNA (miR)-182-5p, and Jumonji domain containing 1A (JMJD1A) were detected by quantitative real-time PCR. ELISA analysis was used to detect inflammatory factor protein expression. Dual-luciferase reporter assay was used to evaluate the targeting relationship between genes.
Results: PCAT19 was continuously upregulated in CCI rats. miR-182-5p was the target of PCAT19, and miR-182-5p was increased after PCAT19 knockdown. NP behaviors such as mechanical ectopic pain and thermal hyperalgesia as well as neuroinflammation can be reduced by knocking down PCAT19. However, the injection of miR-182-5p antagomir significantly reversed the level of the NP behaviors and neuroinflammation caused by PCAT19 knockdown. Besides, dual-luciferase reporter assay showed that JMJD1A was the target gene of miR-182-5p. The level of JMJD1A in CCI rats increased with time. After PCAT19 knockdown, JMJD1A was significantly decreased, but inhibition of miR-182-5p can reverse its levels.
Conclusion: This study shows that PCAT19 plays a role in NP by targeting the miR-182-5p/JMJD1A axis, and PCAT19 can be used as a new therapeutic target for NP.
{"title":"LncRNA PCAT19 Regulates Neuropathic Pain via Regulation of miR-182-5p/JMJD1A in a Rat Model of Chronic Constriction Injury.","authors":"Miao Huo, Xingxing Zheng, Ning Bai, Ruifen Xu, Guang Yang, Ziyu Zhao","doi":"10.1159/000518847","DOIUrl":"https://doi.org/10.1159/000518847","url":null,"abstract":"<p><strong>Introduction: </strong>Neuropathic pain (NP) is one of the most severe chronic pain types. In recent years, more and more studies have shown that long noncoding RNA (LncRNA) plays a key role in a variety of human diseases, including NP. However, the role of LncRNA prostate cancer-associated transcript 19 (PCAT19) in NP and its specific mechanism remain unclear.</p><p><strong>Methods: </strong>A chronic constrictive injury (CCI) rat model was established. Rat paw withdrawal threshold and paw withdrawal latency were used to evaluate the neuronal pain behavior of rats in this model. mRNA expression of PCAT19, neuroinflammatory factor, microRNA (miR)-182-5p, and Jumonji domain containing 1A (JMJD1A) were detected by quantitative real-time PCR. ELISA analysis was used to detect inflammatory factor protein expression. Dual-luciferase reporter assay was used to evaluate the targeting relationship between genes.</p><p><strong>Results: </strong>PCAT19 was continuously upregulated in CCI rats. miR-182-5p was the target of PCAT19, and miR-182-5p was increased after PCAT19 knockdown. NP behaviors such as mechanical ectopic pain and thermal hyperalgesia as well as neuroinflammation can be reduced by knocking down PCAT19. However, the injection of miR-182-5p antagomir significantly reversed the level of the NP behaviors and neuroinflammation caused by PCAT19 knockdown. Besides, dual-luciferase reporter assay showed that JMJD1A was the target gene of miR-182-5p. The level of JMJD1A in CCI rats increased with time. After PCAT19 knockdown, JMJD1A was significantly decreased, but inhibition of miR-182-5p can reverse its levels.</p><p><strong>Conclusion: </strong>This study shows that PCAT19 plays a role in NP by targeting the miR-182-5p/JMJD1A axis, and PCAT19 can be used as a new therapeutic target for NP.</p>","PeriodicalId":19133,"journal":{"name":"Neuroimmunomodulation","volume":null,"pages":null},"PeriodicalIF":2.4,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39413585","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Background: This study aimed to observe the changes of resting energy metabolism in patients with severe neurological diseases, and to explore the effects of tracheostomy status, stroke severity, and complications on resting energy expenditure (REE) and respiratory quotient (RQ).
Methods: A retrospective study was conducted in 105 patients with neurological rehabilitation who were hospitalized in the Rehabilitation Department of the Affiliated Jiangning Hospital of Nanjing Medical University from August 2018 to October 2021. REE was measured by Italian Cosmed k4b2 indirectly, and white blood cell count and C-reactive protein (CRP) were collected.
Results: Among the 105 patients, there were 18 cases of mild stroke, 45 cases of moderate stroke, and 42 cases of severe stroke. The difference between predicted REE and actual REE among different degrees of stroke patients was statistically significant (p < 0.05); there was no significant difference in RQ values among different degrees of stroke patients (p > 0.05). Hemoglobin, albumin, and body mass index were significantly and positively correlated with predicted REE and actual REE, while CRP was significantly negatively correlated with predicted REE and actual REE. There was no significant difference in predicted REE, actual REE, and RQ between renal insufficiency, type 2 diabetes mellitus, and chronic obstructive pulmonary disease (p > 0.05). The CRP level could affect the REE of stroke patients.
Conclusion: Metabolic vehicle assay has a certain clinical value in accurately evaluating the metabolic needs and feeding level of patients.
{"title":"Analysis of Resting Energy Consumption and Its Influencing Factors in Stroke Patients with Severe Neurological Diseases: A Retrospective Clinical Study.","authors":"Hui Feng, Huaping Pan, Wei Yao, Chengyao Mei","doi":"10.1159/000524719","DOIUrl":"https://doi.org/10.1159/000524719","url":null,"abstract":"<p><strong>Background: </strong>This study aimed to observe the changes of resting energy metabolism in patients with severe neurological diseases, and to explore the effects of tracheostomy status, stroke severity, and complications on resting energy expenditure (REE) and respiratory quotient (RQ).</p><p><strong>Methods: </strong>A retrospective study was conducted in 105 patients with neurological rehabilitation who were hospitalized in the Rehabilitation Department of the Affiliated Jiangning Hospital of Nanjing Medical University from August 2018 to October 2021. REE was measured by Italian Cosmed k4b2 indirectly, and white blood cell count and C-reactive protein (CRP) were collected.</p><p><strong>Results: </strong>Among the 105 patients, there were 18 cases of mild stroke, 45 cases of moderate stroke, and 42 cases of severe stroke. The difference between predicted REE and actual REE among different degrees of stroke patients was statistically significant (p < 0.05); there was no significant difference in RQ values among different degrees of stroke patients (p > 0.05). Hemoglobin, albumin, and body mass index were significantly and positively correlated with predicted REE and actual REE, while CRP was significantly negatively correlated with predicted REE and actual REE. There was no significant difference in predicted REE, actual REE, and RQ between renal insufficiency, type 2 diabetes mellitus, and chronic obstructive pulmonary disease (p > 0.05). The CRP level could affect the REE of stroke patients.</p><p><strong>Conclusion: </strong>Metabolic vehicle assay has a certain clinical value in accurately evaluating the metabolic needs and feeding level of patients.</p>","PeriodicalId":19133,"journal":{"name":"Neuroimmunomodulation","volume":null,"pages":null},"PeriodicalIF":2.4,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10394868","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Yong-Ping Zhang, Yu-Yu Li, Cai Zhang, Ya-Jun Li, Bai-Ping Liu, Yan Zhang, Ju-Da Lin, Cai Song
Background: Activated microglia can trigger pro-inflammatory cytokine releases and neuroinflammation, which may inhibit astrocytes to produce neurotrophins and anti-inflammatory factors. Both eventually lead to neuron apoptosis or death. Furthermore, effective antidepressant or anti-dementia treatments can reduce pro-inflammatory cytokines, while enhance interleukin (IL)-10 production. However, the underline mechanism by which IL-10 modulates glial cell function, hence improves cognitive impairment or depression-like behavior is unknown. This study evaluated whether and how IL-10 attenuated chronic IL-1β administration-induced behavioral changes and the possible involved mechanisms.
Methods: Rats received intracerebroventricular injection of IL-1β and/or IL-10 for 14 days. Then animal memory and depression-like behavior, pro-inflammatory cytokines, glial activities, expression of brain-derived neurotrophic factor (BDNF), Trk B, p75, and apoptosis-related genes were studied.
Results: Compared to controls, significantly increased latent time and swimming distance in the Morris-water-maze, decreased sucrose consumption, and decreased locomotor and center zone entries in the open-field were found in rats administrated with IL-1β. These changes were associated with the reduction of GFAP expression, and concentrations of BDNF and anti-inflammatory cytokine IL-10, but the increase in the expressions of CD11b, TrkB, p75, and Caspase-3, the ratio of Bax/Bcl-2, and the concentrations of IL-1β, tumor necrosis factor-α, and IL-6. IL-10 treatment markedly attenuated IL-1β-induced above changes, except for the expressions of neurotrophin receptors.
Conclusion: IL-10-improved behavioral changes may be through suppressing microglia activity and inflammation, while restoring astrocyte function and BDNF expression.
{"title":"Interleukin-10 Attenuates Behavioral, Immune and Neurotrophin Changes Induced by Chronic Central Administration of Interleukin-1β in Rats.","authors":"Yong-Ping Zhang, Yu-Yu Li, Cai Zhang, Ya-Jun Li, Bai-Ping Liu, Yan Zhang, Ju-Da Lin, Cai Song","doi":"10.1159/000521710","DOIUrl":"https://doi.org/10.1159/000521710","url":null,"abstract":"<p><strong>Background: </strong>Activated microglia can trigger pro-inflammatory cytokine releases and neuroinflammation, which may inhibit astrocytes to produce neurotrophins and anti-inflammatory factors. Both eventually lead to neuron apoptosis or death. Furthermore, effective antidepressant or anti-dementia treatments can reduce pro-inflammatory cytokines, while enhance interleukin (IL)-10 production. However, the underline mechanism by which IL-10 modulates glial cell function, hence improves cognitive impairment or depression-like behavior is unknown. This study evaluated whether and how IL-10 attenuated chronic IL-1β administration-induced behavioral changes and the possible involved mechanisms.</p><p><strong>Methods: </strong>Rats received intracerebroventricular injection of IL-1β and/or IL-10 for 14 days. Then animal memory and depression-like behavior, pro-inflammatory cytokines, glial activities, expression of brain-derived neurotrophic factor (BDNF), Trk B, p75, and apoptosis-related genes were studied.</p><p><strong>Results: </strong>Compared to controls, significantly increased latent time and swimming distance in the Morris-water-maze, decreased sucrose consumption, and decreased locomotor and center zone entries in the open-field were found in rats administrated with IL-1β. These changes were associated with the reduction of GFAP expression, and concentrations of BDNF and anti-inflammatory cytokine IL-10, but the increase in the expressions of CD11b, TrkB, p75, and Caspase-3, the ratio of Bax/Bcl-2, and the concentrations of IL-1β, tumor necrosis factor-α, and IL-6. IL-10 treatment markedly attenuated IL-1β-induced above changes, except for the expressions of neurotrophin receptors.</p><p><strong>Conclusion: </strong>IL-10-improved behavioral changes may be through suppressing microglia activity and inflammation, while restoring astrocyte function and BDNF expression.</p>","PeriodicalId":19133,"journal":{"name":"Neuroimmunomodulation","volume":null,"pages":null},"PeriodicalIF":2.4,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10481585","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}