生理学报 Pub Date : 2024-10-25

Yi-Fan Guo, Pei-Ji Chen, Wei-Hua Xiao

{"title":"[Sensory neural innervation of adipose tissue in metabolic disorders].","authors":"Yi-Fan Guo, Pei-Ji Chen, Wei-Hua Xiao","doi":"","DOIUrl":"","url":null,"abstract":"The regulation of adipose tissue homeostasis is essential for maintaining energy and metabolism balance in the body. The peripheral nervous system plays a crucial role in this process. Previous related research primarily focused on the sympathetic nervous system and its release of norepinephrine, while recent attention has shifted to the field of adipose sensory nerves. Studies demonstrate that external stimuli can activate adipose sensory nerves through pathways involving transient receptor potential vanilloid-1 (TRPV1), adipokines, and fatty acids, thereby transmitting signals to the brain. Emerging techniques, such as adipose nerve imaging and denervation of tissues, have revealed the critical role of sensory nerves in the glucose and lipid metabolism, thermogenic function, and vascular regulation of adipose tissue. This article comprehensively reviews the latest research on the regulation and function of sensory nerves in adipose tissue, with a focus on the impact of metabolic diseases on adipose sensory nerves. This review discusses current issues and prospects on the mechanisms behind neural regulation in adipose tissue, hoping to contribute to a comprehensive understanding and providing directions for future research.","PeriodicalId":7134,"journal":{"name":"生理学报","volume":"76 5","pages":"841-848"},"PeriodicalIF":0.0,"publicationDate":"2024-10-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142520688","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}

引用次数: 0

[Research progress of human induced pluripotent stem cells in the establishment and application of dilated cardiomyopathy disease model]. [人类诱导多能干细胞在扩张型心肌病疾病模型建立和应用中的研究进展]。

生理学报 Pub Date : 2024-10-25

Man-Ting Xie, Bing-Bing Xie, Qiu-Ling Xiang

引用次数: 0

A novel positive modulator of GABA_A receptor exhibiting antidepressive properties. 一种新型 GABAA 受体正向调节剂，具有抗抑郁特性。

生理学报 Pub Date : 2024-10-25

Yin-Li Zheng, Fu-Yi Shen, Yang Wang, Jing-Pei Pan, Xian Wang, Tian-Yu Li, Wei-Jia Du, Zhi-Qiang Liu, Yang Li, Fei Guo

{"title":"A novel positive modulator of GABAA receptor exhibiting antidepressive properties.","authors":"Yin-Li Zheng, Fu-Yi Shen, Yang Wang, Jing-Pei Pan, Xian Wang, Tian-Yu Li, Wei-Jia Du, Zhi-Qiang Liu, Yang Li, Fei Guo","doi":"","DOIUrl":"","url":null,"abstract":"γ-Aminobutyric acid (GABA) neurotransmission alterations have been implicated to play a role in depression pathogenesis. While GABAA receptor positive allosteric modulators are emerging as promising in clinical practice, their precise antidepressant mechanism remains to be further elucidated. The aim of the present study was to investigate the effects of LY-02, a novel compound derived from the metabolite of timosaponin, on depression in animals and its mechanism. The results of behavioral tests showed that LY-02 exhibited better antidepressant effects in both male C57BL/6 mice and Sprague Dawley (SD) rats. The results of cellular voltage clamp experiments showed that LY-02 enhanced GABA-mediated currents in HEK293T cells expressing recombinant α6β3δ subunit-containing GABAA receptors. Electrophysiological recording from brain slices showed that LY-02 decreased the amplitude of spontaneous inhibitory postsynaptic current (sIPSC) and increased action potentials of pyramidal neurons in the medial prefrontal cortex (mPFC) of C57BL/6 mice. Western blot results showed that LY-02 dose-dependently up-regulated the protein expression levels of brain-derived neurotrophic factor (BDNF), tropomyosin related kinase B (TrkB) and postsynaptic density protein 95 (PSD-95) in mPFC of mice. The above results suggest that LY-02, as a positive modulator of GABAA receptors, reduces inhibitory neurotransmission in pyramidal neurons. It further activates the BDNF/TrkB signaling pathway, thus exerting antidepressant effects. It suggests that LY-02 is a potential novel therapeutic agent for depression treatment.","PeriodicalId":7134,"journal":{"name":"生理学报","volume":"76 5","pages":"677-690"},"PeriodicalIF":0.0,"publicationDate":"2024-10-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142520693","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}

引用次数: 0

Involvement of mitochondrial TRPV3 in cardiac hypertrophy induced by pressure overload in rats. 线粒体 TRPV3 参与了压力过载诱导的大鼠心肌肥大。

生理学报 Pub Date : 2024-10-25

Mei-Ping Zhu, Bing-Yi Zhang, Ting Lian, Yuan-Jia Tan, Lin-Lin Chang, Pan Xu, Jin-Yi Zhang, Yan-Huan Du, Zhen-Yu Xiong, Qiong Du, Shi-Zhong Zhang

{"title":"Involvement of mitochondrial TRPV3 in cardiac hypertrophy induced by pressure overload in rats.","authors":"Mei-Ping Zhu, Bing-Yi Zhang, Ting Lian, Yuan-Jia Tan, Lin-Lin Chang, Pan Xu, Jin-Yi Zhang, Yan-Huan Du, Zhen-Yu Xiong, Qiong Du, Shi-Zhong Zhang","doi":"","DOIUrl":"","url":null,"abstract":"Mitochondria play an important role in pressure overload-induced cardiac hypertrophy. The present study aimed to investigate the role of mitochondrial transient receptor potential vanilloid 3 (TRPV3) in myocardial hypertrophy. A 0.7 mm diameter U-shaped silver clip was used to clamp the abdominal aorta of Sprague Dawley (SD) rats and establish an animal model of abdominal aortic constriction (AAC). Rat H9C2 myocardial cells were treated with angiotensin II (Ang II) to establish a hypertrophic myocardial cell model, and TRPV3 expression was knocked down using TRPV3 small interfering RNA (siRNA). JC-1 probe was used to detect mitochondrial membrane potential (MMP). DHE probe was used to detect ROS generation. Enzyme activities of mitochondrial respiratory chain complex I and III and ATP production were detected by assay kits. Immunofluorescence staining was used to detect TRPV3 expression in H9C2 cells. Western blot was used to detect the protein expression levels of β-myosin heavy chain (β-MHC), mitochondrial TRPV3 and mitochondrial NOX4. The results showed that, in the rat AAC model heart tissue and H9C2 cells treated with Ang II, the protein expression levels of β-MHC, mitochondrial TRPV3 and mitochondrial NOX4 were up-regulated, MMP was decreased, ROS generation was increased, mitochondrial respiratory chain complex I and III enzyme activities were decreased, and ATP production was reduced. After knocking down mitochondrial TRPV3 in H9C2 cells, the protein expression levels of β-MHC and mitochondrial NOX4 were down-regulated, MMP was increased, ROS generation was decreased, mitochondrial respiratory chain complex I and III enzyme activities were increased, and ATP production was increased. These results suggest that mitochondrial TRPV3 in cardiomyocytes exacerbates mitochondrial dysfunction by up-regulating NOX4, thereby participating in the process of pressure overload-induced myocardial hypertrophy.","PeriodicalId":7134,"journal":{"name":"生理学报","volume":"76 5","pages":"703-716"},"PeriodicalIF":0.0,"publicationDate":"2024-10-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142520694","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}

引用次数: 0

[Research progress on chronic intermittent hypoxia and cognitive impairment]. [慢性间歇性缺氧与认知障碍的研究进展]。

生理学报 Pub Date : 2024-10-25

Ke-Rong Qi, Xue Chen, Jian-Chao Si, Sheng-Chang Yang

引用次数: 0

[The role of oligodendrocyte precursor cells in immunoregulation]. [少突胶质前体细胞在免疫调节中的作用]。

生理学报 Pub Date : 2024-10-25

Xiang Chen, Cheng He, Peng Liu

引用次数: 0

[Research progress of the effects of high-intensity interval training on excess post-exercise oxygen consumption in human]. [高强度间歇训练对人体运动后多余耗氧量影响的研究进展]。

生理学报 Pub Date : 2024-10-25

Yang-Yang Su, Xiao-Ning Dong, Xiu-Qin Wu

{"title":"[Research progress of the effects of high-intensity interval training on excess post-exercise oxygen consumption in human].","authors":"Yang-Yang Su, Xiao-Ning Dong, Xiu-Qin Wu","doi":"","DOIUrl":"","url":null,"abstract":"Elevated human metabolism during recovery is associated with increased excess post-exercise oxygen consumption (EPOC). EPOC is linearly related to exercise duration and exponentially related to exercise intensity. It is commonly believed that near-maximal intensity interval training prompts the body to produce greater EPOC. This review focuses on the origin and development of high-intensity interval training (HIIT), analyzes its concept, classification and function, and discusses its effects on human EPOC. HIIT promotes a significant increase in EPOC during the fast recovery period, whereas the changes of EPOC during the slow recovery period are still inconclusive; Sprint interval training (SIT) promotes a significant increase in EPOC throughout the whole recovery period. Compared with HIIT, the body's energy expenditure and oxygen uptake (VO2) increase significantly during moderate-intensity continuous training (MICT), but the total energy expenditure and VO2 during exercise and 24 h of recovery period are similar between the two types of exercises, indicating that greater EPOC is generated during the recovery period of HIIT. The mechanisms by which interval training improves EPOC include increasing lung ventilation and catecholamine secretion, accelerating systemic circulation, increasing body temperature, promoting glycogen resynthesis, rapid recruitment of fast twitch muscle fibers and uncoupling of mitochondrial respiration, up-regulating hypoxia inducible factor-1 alpha and skeletal muscle protein, as well as improving intestinal flora.","PeriodicalId":7134,"journal":{"name":"生理学报","volume":"76 5","pages":"849-861"},"PeriodicalIF":0.0,"publicationDate":"2024-10-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142520683","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}

引用次数: 0

Role of voltage-gated potassium channel α subunits in cardiovascular system. 电压门控钾通道 α 亚基在心血管系统中的作用

生理学报 Pub Date : 2024-10-25

Jin-Ru Yang, Peng Huang, Shu-Kuan Ling

引用次数: 0

[Exogenous EPO protects HT22 cells from intermittent hypoxia-induced injury by activating JAK2-STAT5 signaling pathway]. [外源性 EPO 通过激活 JAK2-STAT5 信号通路保护 HT22 细胞免受间歇性缺氧诱导的损伤】。］

生理学报 Pub Date : 2024-10-25

Ke-Rong Qi, Xue Chen, Jian-Chao Si, Qing-Qing Liu, Sheng-Chang Yang

{"title":"[Exogenous EPO protects HT22 cells from intermittent hypoxia-induced injury by activating JAK2-STAT5 signaling pathway].","authors":"Ke-Rong Qi, Xue Chen, Jian-Chao Si, Qing-Qing Liu, Sheng-Chang Yang","doi":"","DOIUrl":"","url":null,"abstract":"The aim of this study was to investigate the effects of exogenous erythropoietin (EPO) on intermittent hypoxia (IH)-induced neuronal injury and the underlying mechanism. Mouse hippocampal neuron HT22 cells were exposed to IH for different durations (1% O2 for 7 min/21% O2 for 3 min, one cycle for 10 min). Cell viability was detected by CCK-8. EPO content in the supernatant of cell culture medium was detected by ELISA kit, and the protein expression was detected by Western blot. EPO receptor (EPOR) protein expression was detected by immunofluorescence staining and Western blot. Cellular apoptosis and mitochondrial membrane potential were detected by the corresponding kits. Reactive oxygen species (ROS) level was detected by DCFH probe, and expression levels of JAK2-STAT5 signaling pathway-related proteins were detected by Western blot. The results showed that IH exposure significantly decreased HT22 cell activity. EPO and EPOR protein expressions were significantly up-regulated at 12 h of IH exposure, but down-regulated at 24 and 48 h. In IH-treated HT22 cells, exogenous EPO significantly increased cell activity and mitochondrial membrane potential, decreased ROS levels and cell apoptosis, up-regulated Nrf-2 and heme oxygenase 1 (HO-1) protein expression levels, decreased Cleaved-Caspase-3/Caspase-3 and Bax/Bcl-2 ratios, and promoted the phosphorylation of JAK2-STAT5 pathway-related proteins. Whereas JAK2 and STAT5 blockers both reversed these neuronal protective effects of EPO. These results suggest exogenous EPO inhibits IH-induced oxidative stress and apoptosis by activating the JAK2-STAT5 signaling pathway, thus exerting a neuronal protective effect.","PeriodicalId":7134,"journal":{"name":"生理学报","volume":"76 5","pages":"691-702"},"PeriodicalIF":0.0,"publicationDate":"2024-10-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142520679","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}

引用次数: 0

[Research progress on the mechanism of autophagy flow injury caused by lysosomal dysfunction after cerebral ischemia]. [脑缺血后溶酶体功能障碍导致自噬流损伤机制的研究进展]。

生理学报 Pub Date : 2024-10-25

Jia-Qian Wang, Hong-Yun He, Yi-Hao Deng

{"title":"[Research progress on the mechanism of autophagy flow injury caused by lysosomal dysfunction after cerebral ischemia].","authors":"Jia-Qian Wang, Hong-Yun He, Yi-Hao Deng","doi":"","DOIUrl":"","url":null,"abstract":"Ischemic stroke is an acute cerebrovascular disease caused by cerebral vascular obstruction, which is the third leading cause of human death and disability. Multiple studies have demonstrated that autophagy plays a positive role in neurons after ischemic stroke. Autophagy is the main intracellular mechanism that mediates the degradation and recycling of various substrates in lysosomes, so it is very important to maintain normal function of lysosomes. However, cerebral ischemia can result in significant impairment of lysosomal function, subsequently leading to disruption in autophagy flow and exacerbation of neuronal injury. This review elucidates the mechanism of autophagic flux injury resulting from lysosomal dysfunction induced by impaired fusion between autophagosomes and lysosomes, alterations in the acidic environment within lysosomes, and diminished biosynthesis of lysosomes following ischemic stroke. The lysosome is regarded as the primary focal point for investigating the mechanism of autophagic flux injury, with the aim of modulating neuronal autophagic flux to improve cerebral ischemia-induced brain injury. This approach holds potential for exerting a neuroprotective effect and providing a novel avenue for stroke treatment.","PeriodicalId":7134,"journal":{"name":"生理学报","volume":"76 5","pages":"783-790"},"PeriodicalIF":0.0,"publicationDate":"2024-10-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142520686","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}

引用次数: 0

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