Acta Physiologica Sinica (APS) is sponsored by the Chinese Association for Physiological Sciences and Shanghai Institutes of Biological Sciences, Chinese Academy of Sciences (CAS), and is published bimonthly by the Science Press, China. APS publishes original research articles in the field of physiology as well as research contributions from other biomedical disciplines and proceedings of conferences and symposia of physiological sciences. Besides “Original Research Articles”, the journal also provides columns as “Brief Review”, “Rapid Communication”, “Experimental Technique”, and “Letter to the Editor”. Articles are published in either Chinese or English according to authors’ submission.

Acta Physiologica Sinica (APS) is sponsored by the Chinese Association for Physiological Sciences and the Shanghai Institutes of Biological Sciences, Chinese Academy of Sciences (CAS). It is published bimonthly by Science Press, China. APS primarily publishes original research articles in the field of physiology, as well as contributions from other biomedical disciplines and proceedings from conferences and symposia related to physiological sciences. In addition to 'Original Research Articles', the journal features columns such as 'Brief Review', 'Rapid Communication', 'Experimental Technique', and 'Letter to the Editor'. Articles are published in either Chinese or English, depending on the authors' submission.

《Acta Physiologica Sinica》由中国生理科学学会和中国科学院上海生命科学研究院主办，由科学出版社出版，发行频率为双月刊。该期刊主要发表生理学领域的原创研究文章，同时也欢迎其他生物医学学科的研究贡献，以及生理科学会议和研讨会的论文集。除了“原创研究文章”，期刊还设有“简评”、“快速通讯”、“实验技术”和“致编辑的信”等栏目。文章可以根据作者的提交选择中文或英文发表。

Acta Physiologica Sinica

The apoptosis of nucleus pulposus cells (NPCs) is the main cellular process of intervertebral disc degeneration (IVDD). Our previous studies showed that 17β-estradiol (E2) protects rat NPCs from interleukin-1β (IL-1β)-induced apoptosis via the PI3K/Akt signaling pathway. This study was aimed to investigate whether downstream proteins of PI3K/Akt pathway were involved in inhibition of E2 on NPCs' apoptosis. Primary culture of rat NPCs was isolated by trypsin digestion. Being pretreated with E2 and different inhibitors of downstream proteins of PI3K/Akt pathway, the NPCs were treated with IL-1β. Cellular apoptosis was detected by Annexin V/PI staining. Cell viability was detected by CCK-8. Cell adhesion was evaluated by cell-collagen binding assay. Phosphorylation levels of mammalian target of Rapamycin (mTOR), glycogen synthase kinase-3β (GSK-3β) and nuclear factor κB (NF-κB) were detected by Western blot. The results showed that E2 significantly inhibited the IL-1β-induced apoptosis of NPCs, reversed the decrease of cell viability and adhesion induced by IL-1β, and inhibited the down-regulation of mTOR phosphorylation level induced by IL-1β. Rapamycin could block these protective effects of E2. These results suggest that E2 may inhibit IL-1β-induced NPCs' apoptosis through the PI3K/Akt/mTOR signaling pathway.

Hong-Tao Guo

Er-Fei Guo

Jian-Jie Xu

Bin Zhang

Yan-Bing Gao

Jian-Zhong Wu

Shengli xuebao

[17β-estradiol inhibits interleukin-1β-induced rat nucleus pulposus cell apoptosis through the PI3K/Akt/mTOR signal pathway].

[17β-雌二醇通过PI3K/Akt/mTOR信号通路抑制白细胞介素-1β诱导的大鼠髓核细胞凋亡]

This study was designed to evaluate the role of short-chain fatty acid butyrate acid on intestinal morphology and function, and atherosclerotic plaque formation in apolipoprotein E-knockout (ApoE-/-) mice. ApoE-/- mice on high-fat, high-cholesterol diet were treated with butyrate acid (200 mmol/L) or NaCl (control) in the drinking water for 12 weeks, followed by histological evaluations of atherosclerotic lesion in aorta. Real-time PCR analysis and ELISA were used to measure the expression levels of proinflammatory cytokines. Butyrate acid significantly attenuated high-fat, high-cholesterol diet-induced atherosclerotic plaque formation in ApoE-/- mice. Butyrate acid prevented high-fat, high-cholesterol diet-induced inflammation in both the aorta and the circulation, as evidenced by reduced expression of proinflammatory cytokines. These changes were accompanied by a marked attenuation in metabolic endotoxemia lipopolysaccharide (LPS). Butyrate acid induced intestinal expression of the tight junction proteins (Occludin and zona occuldens protein-1), thereby preventing the gut permeability. Butyrate acid dose-dependently upregulated the expression of the tight junction proteins in Caco-2 cells in GPR41-dependent manner. In conclusion, butyrate acid attenuates atherosclerotic lesions by ameliorating metabolic endotoxemia-induced inflammation through restoration of the gut barrier.

Hong-Bo Bai

Ping Yang

Han-Bin Zhang

Yu-Lin Liu

Shu-Xiang Fang

Xiao-Yang Xu

[Short-chain fatty acid butyrate acid attenuates atherosclerotic plaque formation in apolipoprotein E-knockout mice and the underlying mechanism].

[短链脂肪酸丁酸减轻载脂蛋白E敲除小鼠动脉粥样硬化斑块形成及其机制]

In eukaryotic cells, the endoplasmic reticulum (ER) is the key quality control organelle for cellular protein synthesis and processing. It also serves as an important site for Ca2+ storage and lipid biosynthesis. In response to a variety of external stimuli, a cellular unfolded protein response (UPR) is activated to handle ER stress caused by increased accumulation of unfolded or misfolded proteins at the ER. The UPR plays a crucial role in maintaining ER homeostasis and cell functions. Three ER-localized transmembrane proteins, inositol-requiring enzyme 1α (IRE1α), PKR-like ER kinase (PERK), and activating transcription factor 6 (ATF6), act to sense ER stress and mediate three canonical UPR signaling pathways. Besides restoring the protein folding capability to relieve ER stress, the UPR pathways have also been implicated in the regulation of cell metabolism and energy balance. In the state of overnutrition, ER stress has been documented to occur in adipose tissue that has a key role in energy storage and consumption. As an endocrine organ, adipose tissue regulates glucose and lipid metabolism through secreting adipocyte cytokines, and it undergoes metabolic inflammation during pathogenic development of obesity, insulin resistance and type 2 diabetes. In this review, we attempt to summarize the recent progress with regard to the UPR regulation of adipose tissue physiology. We wish to focus upon the mechanism by which ER stress response is linked to adipose tissue dysfunction, hoping to promote our current understanding of UPR signaling in the pathophysiology of obesity and related metabolic diseases.

Yu-Rong Hu

Yong Chen

Yong Liu

Role of endoplasmic reticulum stress response in regulation of adipose tissue metabolism

内质网应激反应在调节脂肪组织代谢中的作用

Astrocytes are a heterogenous group of macroglia present in all regions of the brain and play critical roles in many aspects of brain development, function and disease. Previous studies suggest that the B-cell lymphoma-2 associated X protein (BAX)-dependent apoptosis plays essential roles in regulating neuronal number and achieving optimal excitation/inhibition ratio. The aim of the present paper was to study whether BAX regulates astrocyte distribution in a region-specific manner. Immunofluorescence staining of SOX9 was used to analyze and compare astrocyte density in primary somatosensory cortex, motor cortex, retrosplenial cortex and hippocampus in heterozygous and homozygous BAX knockout mice at age of six weeks when cortical development has finished and glia development has reached a relatively steady state. The results showed that astrocyte density varied significantly among different cortical subdivisions and between cortex and hippocampus. In contrast to the significant increase in GABAergic interneurons, the overall and region-specific astrocyte density remained unchanged in the cortex when BAX was absent. Interestingly, a significant reduction of astrocyte density was observed in the hippocampus of BAX knockout mice. These data suggest that BAX differentially regulates neurons and astrocytes in cortex as well as astrocytes in different brain regions during development. This study provided important information about the regional heterogeneity of astrocyte distribution and the potential contribution of BAX gene during development.

Li-Fang Zhu

Xiao-Yang Wu

Xue Liu

Liang Ma

Qi Zhang

Zi Yu

Zhi-Jiao He

Yue Ying

Zhu-Tian Zhang

Xiao-Yu Pan

Yu-Qi Cai

Ling Gong

Miao He

Absence of BAX differentially affects astrocyte density in the mouse cortex and hippocampus

BAX缺失对小鼠皮层和海马神经胶质细胞密度影响不同

The research on the molecular mechanism of vascular injury has been a hot topic in recent years since the mechanism can be targeted for the treatment of vascular injury diseases. A large number of studies have found that vascular injury, repair and pathological remodeling are closely related to phenotype switching, abnormal proliferation and migration, and apoptosis of vascular smooth muscle cells (VSMCs). Smooth muscle 22α (SM22α) is a shape change and transformation sensitive F-actin-binding protein. SM22α decorates the contractile filament bundles within cultured VSMCs exhibiting differentiated phenotypes. In addition, SM22α is involved in regulation of cell signaling pathways related to vascular homeostasis and vascular remodeling. Here, we reviewed the recent research progress of SM22α in vascular homeostasis and remodeling.

Ning Zhang

Yong-Qing Dou

Mei Han

Roles of smooth muscle 22α in vascular homeostasis and vascular remodeling

平滑肌22α在血管稳态和血管重塑中的作用

β3-adrenergic agonists induce adaptive thermogenesis and promote beiging of white fat. However, it remains unclear which metabolites mediate the stimulatory effects of β3-adrenergic agonists on thermogenesis of brown and beige fat. In this study, adipose tissue was isolated from 8-week-old C57/BL6J male mice by intraperitoneal administration of β3-adrenergic agonist CL316,243 for RNA-Seq, which revealed that histidine decarboxylase, a key enzyme in histamine synthesis, was strongly induced in adipose by CL316,243. Therefore, we speculated that histamine might be involved in the process of thermogenesis in adipose tissue. We determined the physiological role and mechanism by which histamine promotes fat thermogenesis by intravenous administering histamine to C57BL/6J mice fed a normal or a high-fat diet. The results showed that intravenous injection of histamine into C57BL/6J mice fed a normal diet stimulated the expression of thermogenic genes, including peroxisome proliferator-activated receptor gamma coactivator-1α (PGC-1α) and uncoupling protein 1 (UCP1), in brown adipose tissue (BAT) and inguinal white adipose tissue (iWAT). H&E staining also suggested that histamine treatment decreased the size of lipid droplets in adipocytes. Moreover, histamine treatment also enhanced thermogenesis of fat in high-fat diet induced obese mice, and improved glucose intolerance and fatty liver phenotype. Finally, we demonstrated that the effects of histamine on the thermogenic program were cell autonomous. Our data suggest that histamine may mediate the effects of β3-adrenergic agonists on thermogenesis of fat.

Yue-Yao Feng

Yu-Jie Zhang

Yong-Sheng Chang

Histamine stimulates thermogenesis of brown and beige fat

组胺刺激棕色和米色脂肪的产热作用

The present study was aimed to explore the correlation between θ-γ neural oscillations phase-amplitude coupling (PAC) in hippocampal CA3 area and the changes of spatial identifying and cognitive ability before and after shock avoidance training in rats. According to the results of Y-type maze shock avoidance training, the rats were divided into two groups: the fast avoidance response group and the general avoidance response group. The local field potential (LFP) of hippocampal CA3 area was recorded by wireless telemetry before and after shock avoidance training. The variation of θ oscillation (3-7 Hz) and low-γ neural oscillation (30-60 Hz) PAC in hippocampal CA3 area was analyzed by MATLAB wavelet packet extraction technique. The results showed that, compared with the general avoidance response group, the fast avoidance response group exhibited higher θ-γ neural oscillation PAC in hippocampal CA3 area before training. θ-γ oscillation PAC in hippocampal CA3 area was increased in both groups after training. It was also noticed that θ-γ neural oscillation PAC of some frequency bands in the general avoidance response group were significantly higher than those in the fast avoidance response group. The results suggest that certain intensity of training can change the spatial identifying and cognitive ability of rats, and the mechanism may involve the increase of the synchrony of θ-γ neural oscillation, i.e., the enhancement of θ-γ phase-amplitude alternating frequency coupling in hippocampal neurons.

Min Li

Zheng Ye

Zai-Man Zhu

Ke-Yu Liu

Xiao-Yan Sun

Hao Meng

[Correlation between theta-gamma neural oscillations in hippocampal CA3 area and the spatial identifying and cognitive ability in rats].

[海马CA3区theta-gamma神经振荡与大鼠空间识别和认知能力的相关性]

The high failure rate of the new drug development has been well recognized. Relying on the pre-clinical data obtained from animal experiments will inevitably cause a low concordance with human clinical trials, which will eventually lead to new drug development failure. Employing human induced pluripotent stem cells (iPSCs) or adult stem cells to simulate disease models can not only provide an unlimited cell materials, but also faithfully represent the genetic background of a certain disease, when iPSCs or adult stem cells derived from patients with a specific disease genetic variation are applied. In addition, gene editing methods can be used to introduce genetic variants of interest into stem cells to generate disease models. Furthermore, by establishing a cell bank with a population of iPSCs in petri dish, in vitro human genetic studies can be carried out in these cells, with GWAS and QTL studies applied to identify genetic variants that are associated with drug sensitivity or cytotoxicity. These efforts may offer valuable information for the recruitment of suitable patients for clinical trials. Therefore, stem cell-derived disease models can provide valuable resources for the pathophysiological studies of diseases as well as the drug development. In this review, we will briefly introduce the development of the liver disease models derived from stem cells and their applications in disease study and drug development.

Xiao-Shan Wu

Shuang Li

Qiu-Rong Ding

Applications of stem cell disease models in liver metabolic research and drug development

干细胞疾病模型在肝脏代谢研究和药物开发中的应用

The mitochondrial unfolded protein response is an important component of the mitochondrial protein quality control program. It can effectively remove unfolded or misfolded proteins under stress, and maintain a stable and healthy mitochondrial pool. The mitochondrial unfolded protein response is coordinated by multiple signaling pathways. The classical ATF4/ATF5-CHOP pathway is induced by accumulation of unfolded or misfolded proteins in the mitochondrial matrix, which reduces stress toxicity by regulating molecular chaperones and proteases. Sirt3-FOXO3a-SOD2 pathway, located in the mitochondrial matrix, plays an important role in anti-oxidative damage. The ERα-NRF1-HTRA2 pathway mainly removes unfolded proteins in the mitochondrial membrane space and improves the quality control of mitochondrial proteins. These three signaling pathways work both independently and cooperatively to enhance mitochondrial capacity and maintain health under stress.

Chun-Wei Ma

Bing-Hong Gao

Unfolded protein response signaling in mitochondria

线粒体中的未折叠蛋白反应信号传导

Follicle-stimulating hormone (FSH) was once thought to play a role only in reproduction, promoting follicle development and maturation in women and spermgenesis in men. However, in recent ten years, FSH has been found to have new functions on metabolic regulation and aging. FSH regulates bone formation, fat metabolism, energy homeostasis, cholesterol production and cardiovascular disease by binding with its receptor FSHR. These newly discovered regulatory roles of FSH are exciting, as it is suggested that blocking FSH may have potential translational impacts on treatments of a series of age-related diseases, including osteoporosis, obesity, dyslipidemia, cardiovascular disease.

Cai-Xia Zhao

Peng Liu

[Follicle-stimulating hormone: new roles in metabolic regulation and aging].

[促卵泡激素：代谢调控与衰老中的新角色]

ISSN	0371-0874
h-index	29

Publication Information	Publisher: Kexue Chubaneshe/Science Press，Publishing cycle: ，Journal Type: journal，Open Access Journals: No
Basic data	Year of publication: 2023，Proportion of original research papers: 0.00%，Self Citation Rate:N.A.， Gold OA Rate: 0.00%

Acta Physiologica Sinica

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