Chinese Journal of Physiology最新文献_第7页

The role of exercise intensity on fatty liver in rats. 运动强度对大鼠脂肪肝的影响。

IF 1.8 4区医学

Chinese Journal of Physiology Pub Date : 2022-11-01 DOI: 10.4103/0304-4920.365461

Xueyan Gu, Xiaocui Ma, Limin Mo, Qiyu Wang

{"title":"The role of exercise intensity on fatty liver in rats.","authors":"Xueyan Gu, Xiaocui Ma, Limin Mo, Qiyu Wang","doi":"10.4103/0304-4920.365461","DOIUrl":"https://doi.org/10.4103/0304-4920.365461","url":null,"abstract":"Nonalcoholic fatty liver disease (NAFLD) is the most common chronic liver disease and is often caused by obesity. Currently, moderate-intensity continuous training (MICT) and high-intensity interval training (HIIT) are two effective treatments for reducing fat mass in patients with obesity and NAFLD. However, the comparative fat-reducing effects and underlying molecular mechanisms of MICT and HIIT remain unclear. This comprehensive study was performed on male Wistar rats treated with standard diet, high-fat diet, MICT, and HIIT to explore their comparative fat-reducing effects and corresponding molecular mechanisms. HIIT had a greater effect on hepatic vacuolation density and lipid content reduction than MICT, and triglyceride and total cholesterol levels in the serum and the liver demonstrated different sensitivities to different exercise training programs. At the molecular level, both MICT and HIIT altered the processes of fatty acid synthesis, fatty acid transport, fatty acid β-oxidation, and cholesterol synthesis, wherein the transcriptional and translational levels of signaling molecules peroxisome proliferator-activated receptors (PPARs) regulating fatty acid and cholesterol synthesis were strongly changed. Moreover, the metabolic pathways of amino acids, bile acids, and carbohydrates were also affected according to transcriptome analysis, and the changes in the above-mentioned processes in the HIIT group were greater than those in the MICT group. In combination with the search tool for the retrieval of interacting genes/proteins (STRING) analysis and the role of PPARs in lipid metabolism, as well as the expression pattern of PPARs in the MICT and HIIT groups, the MICT-and HIIT-induced fat loss was mediated by the PPAR pathway, causing feedback responses in fatty acid, steroid, amino acid, bile acid, and carbohydrate metabolism, and HIIT had a better fat-reducing effect, which may be initiated by PPAR-α. This study provides a theoretical basis for targeted therapy of patients with obesity and NAFLD.","PeriodicalId":10251,"journal":{"name":"Chinese Journal of Physiology","volume":"65 6","pages":"301-310"},"PeriodicalIF":1.8,"publicationDate":"2022-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10466566","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}

引用次数: 1

Optimization of exercise preconditioning duration in protecting from exhausted exercise-induced cardiac injury in rats. 优化运动预处理时间对大鼠运动性心力损伤的保护作用。

IF 1.8 4区医学

Chinese Journal of Physiology Pub Date : 2022-11-01 DOI: 10.4103/0304-4920.365457

Zheng Ping, Jinyu Li, Yawei Sun, Xiaoli Zhang, Ziwen Wang, Xuebin Cao

{"title":"Optimization of exercise preconditioning duration in protecting from exhausted exercise-induced cardiac injury in rats.","authors":"Zheng Ping, Jinyu Li, Yawei Sun, Xiaoli Zhang, Ziwen Wang, Xuebin Cao","doi":"10.4103/0304-4920.365457","DOIUrl":"https://doi.org/10.4103/0304-4920.365457","url":null,"abstract":"The effect of different duration of exercise preconditioning (EP) on protecting from exhaustive exercise-induced cardiac injury (EECI) has been optimized in rats. Male Sprague-Dawley rats were divided into six groups: the control group, exhaustive exercise (EE) group, EP 20-min + EE group, EP 40-min + EE group, EP 60-min + EE group and EP 80-min + EE group. The EP groups were subjected to treadmill running at the intensity of 74.0% V̇O2 max. Changes of exercise capacity, cardiac pathology, myocardial enzymology, electrocardiogram (ECG), cardiac function, and mitochondrial respiratory function were compared. Compared to the C group, the EE group has shown significant decrease of exercise capacity, elevation of serum N-terminal pro B-type natriuretic peptide (NT-proBNP) and cardiac troponin-I (cTn-I) levels, cardiac morphology change, ECG disturbance, cardiac dysfunction and reduction of myocardial mitochondrial respiration function. Compared to the EE group, the EP groups have shown significant elevation of exercise capacity, decrease of serum NT-proBNP and cTn-I, improvement of cardiac function and myocardial mitochondrial electron transfer pathway complex I, II and IV activity. The correlation analyses showed protection of EP was proportional to EP duration from 20-min to 60-min. EE caused cardiac injury. EP could protect from EECI by alleviating myocardial damage, improving cardiac function and mitochondrial ETP complex I, II and IV activity. EP protection was positively correlated to EP duration from 20-min to 60-min with EP intensity fixed at 74.0% V̇O2 max.","PeriodicalId":10251,"journal":{"name":"Chinese Journal of Physiology","volume":"65 6","pages":"290-300"},"PeriodicalIF":1.8,"publicationDate":"2022-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10466567","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}

引用次数: 0

Overexpression of long non-coding RNA LINC00158 inhibits neuronal apoptosis by promoting autophagy in spinal cord injury. 长链非编码RNA LINC00158过表达通过促进脊髓损伤自噬抑制神经元凋亡。

IF 1.8 4区医学

Chinese Journal of Physiology Pub Date : 2022-11-01 DOI: 10.4103/0304-4920.360035

Fuchuang Qin, Guorong He, Yu Sun, Guangning Chen, Qijian Yu, Xilie Ma

{"title":"Overexpression of long non-coding RNA LINC00158 inhibits neuronal apoptosis by promoting autophagy in spinal cord injury.","authors":"Fuchuang Qin, Guorong He, Yu Sun, Guangning Chen, Qijian Yu, Xilie Ma","doi":"10.4103/0304-4920.360035","DOIUrl":"https://doi.org/10.4103/0304-4920.360035","url":null,"abstract":"Spinal cord injury (SCI) is a common central nervous system disease. It is reported that long non-coding RNA LINC00158 is involved in the process of SCI. The purpose of this study was to explore the biological role of LINC00158 in the SCI. First, we established a rat SCI model by surgical method and evaluated the motor function of rats by the Basso-Beattie-Bresnahan locomotor rating scale. The results showed that the expression of LINC00158 decreased and apoptotic cells increased in the SCI model rats. Meanwhile, we found the upregulated LC3-II/LC3-I, Beclin-1, and p62 in the SCI rats. Then, primary rat spinal cord neurons were exposed to oxygen/glucose deprivation (OGD) as an in vitro cell model of SCI. After OGD treatment, the expression of LINC00158 decreased significantly and the apoptosis of spinal cord neurons increased. OGD treatment resulted in upregulation of LC3-II/LC3-I and Beclin-1 and downregulation of p62 in primary spinal cord neurons, which could be eliminated by overexpression of LINC00158. 3-Methyladenine and chloroquine (autophagy inhibitor) reversed the inhibitory effect of LINC00158 overexpression on apoptosis of primary spinal cord neurons. In conclusion, this study demonstrated that LINC00158 overexpression repressed neuronal apoptosis by promoting autophagy, suggesting that LINC00158 may be a potential therapeutic target in the SCI.","PeriodicalId":10251,"journal":{"name":"Chinese Journal of Physiology","volume":"65 6","pages":"282-289"},"PeriodicalIF":1.8,"publicationDate":"2022-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10522917","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}

引用次数: 1

Sensitivity of Ca²⁺-sensing receptor-transient receptor potential-mediated Ca²⁺ influx to extracellular acidity in bEND.3 endothelial cells. Ca2+感应受体-瞬时受体电位介导的Ca2+内流对弯曲细胞外酸度的敏感性。3个内皮细胞。

IF 1.8 4区医学

Chinese Journal of Physiology Pub Date : 2022-11-01 DOI: 10.4103/0304-4920.365460

Iat-Lon Leong, Chung-Ming Yu, Lian-Ru Shiao, Paul Chan, King-Chuen Wu, Yuk-Man Leung

{"title":"Sensitivity of Ca2+-sensing receptor-transient receptor potential-mediated Ca2+ influx to extracellular acidity in bEND.3 endothelial cells.","authors":"Iat-Lon Leong, Chung-Ming Yu, Lian-Ru Shiao, Paul Chan, King-Chuen Wu, Yuk-Man Leung","doi":"10.4103/0304-4920.365460","DOIUrl":"https://doi.org/10.4103/0304-4920.365460","url":null,"abstract":"Ca2+-sensing receptors (CaSRs) are G protein-coupled receptors activated by elevated concentrations of extracellular Ca2+. In our previous works, we showed protein and functional expression of CaSR in mouse cerebral endothelial cell (EC) (bEND.3); the CaSR response (high Ca2+-elicited cytosolic [Ca2+] elevation) was unaffected by suppression of phospholipase C but in part involved Ca2+ influx through transient receptor potential V1 (TRPV1) channels. In this work, we investigated if extracellular acidity affected CaSR-mediated Ca2+ influx triggered by high (3 mM) Ca2+ (CaSR agonist), 3 mM spermine (CaSR agonist), and 10 mM cinacalcet (positive allosteric modulator of CaSR). Extracellular acidosis (pH 6.8 and pH 6.0) strongly suppressed cytosolic [Ca2+] elevation triggered by high Ca2+, spermine, and cinacalcet; acidosis also inhibited Mn2+ influx stimulated by high Ca2+ and cinacalcet. Purinoceptor-triggered Ca2+ response, however, was not suppressed by acidosis. Extracellular acidity also did not affect membrane potential, suggesting suppressed CaSR-mediated Ca2+ influx in acidity did not result from the reduced electrical driving force for Ca2+. Our results suggest Ca2+ influx through a putative CaSR-TRP complex in bEND.3 EC was sensitive to extracellular pH.","PeriodicalId":10251,"journal":{"name":"Chinese Journal of Physiology","volume":"65 6","pages":"277-281"},"PeriodicalIF":1.8,"publicationDate":"2022-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10522918","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}

引用次数: 0

Leonurine suppresses prostate cancer growth in vitro and in vivo by regulating miR-18a-5p/SLC40A1 axis. 益母鼠尿通过调控miR-18a-5p/SLC40A1轴抑制前列腺癌体外和体内生长。

IF 1.8 4区医学

Chinese Journal of Physiology Pub Date : 2022-11-01 DOI: 10.4103/0304-4920.365459

Bin Liang, Shouxi Cui, Songnian Zou

引用次数: 2

Study on the role of naringin in attenuating Trimethylamine-N-Oxide-Induced human umbilical vein endothelial cell inflammation, oxidative stress, and endothelial dysfunction. 柚皮苷对三甲胺- n -氧化物诱导的人脐静脉内皮细胞炎症、氧化应激和内皮功能障碍作用的研究。

IF 1.8 4区医学

Chinese Journal of Physiology Pub Date : 2022-09-01 DOI: 10.4103/0304-4920.359796

Hui Zhao, Jianping Zhao

{"title":"Study on the role of naringin in attenuating Trimethylamine-N-Oxide-Induced human umbilical vein endothelial cell inflammation, oxidative stress, and endothelial dysfunction.","authors":"Hui Zhao, Jianping Zhao","doi":"10.4103/0304-4920.359796","DOIUrl":"https://doi.org/10.4103/0304-4920.359796","url":null,"abstract":"Trimethylamine-N-oxide (TMAO), a phospholipid metabolite, can modulate cholesterol synthesis and promote vascular inflammation and endothelial dysfunction, thereby increasing the risk of atherosclerosis (AS). Previously, it was found that naringin reduced damage to human umbilical vein endothelial cells (HUVECs) triggered by oxidized low-density lipoprotein. This article continues to explore the role and mechanism of naringin in protecting HUVECs from TMAO-induced damage. After the construction of TMAO-induced AS model in HUVECs, inflammation, oxidative stress, and endothelial function were examined by real-time quantitative polymerase chain reaction, Western blotting, nitric oxide (NO), reactive oxygen species (ROS), superoxide dismutase, and malondialdehyde (MDA) kits. Results showed that naringin pretreatment inhibited endothelial inflammation and oxidative stress, promoted NO release, and inhibited the degradation of Zona occludens-2, occludin, and vascular endothelial-cadherin, thereby restoring the functional and structural integrity of the endothelium. Furthermore, the addition of mitogen-activated protein kinase (MAPK) agonist demonstrated that the therapeutic effect of naringin was achieved through inactivating TMAO-stimulated MAPK signaling in HUVECs.","PeriodicalId":10251,"journal":{"name":"Chinese Journal of Physiology","volume":"65 5","pages":"217-225"},"PeriodicalIF":1.8,"publicationDate":"2022-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40456071","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}

引用次数: 1

Effects of dietary triiodothyronine or dopamine on small intestinal oxygen consumption in chicks. 饲粮中添加三碘甲状腺原氨酸或多巴胺对雏鸡小肠耗氧量的影响。

IF 1.8 4区医学

Chinese Journal of Physiology Pub Date : 2022-09-01 DOI: 10.4103/0304-4920.359798

Shen-Chang Chang, Yang-Kwang Fan, Shao-Yu Peng, Min-Jung Lin

{"title":"Effects of dietary triiodothyronine or dopamine on small intestinal oxygen consumption in chicks.","authors":"Shen-Chang Chang, Yang-Kwang Fan, Shao-Yu Peng, Min-Jung Lin","doi":"10.4103/0304-4920.359798","DOIUrl":"https://doi.org/10.4103/0304-4920.359798","url":null,"abstract":"This study aimed to investigate the effects of triiodothyronine (T3)- or dopamine (Dp)-supplemented diets on oxygen consumption by Na+, K+-ATPase activity in broiler chicks. Five groups, each with twenty-four 6-day-old chicks, randomly received one of the five dietary treatments: (1) Basal diet (commercial broiler rations with 23.0% crude protein and 3,133 kcal metabolizable energy/kg) or CON, (2) basal diet plus 0.7 μmol Dp/kg diet or Dp0.7, (3) basal diet plus 2.4 μmol Dp/kg diet or Dp2.4, (4) basal diet plus 1.9 μmol T3/kg diet or T1.9, and (5) basal diet plus 3.8 μmol T3/kg diet or T3.8 from 6 to 14 days of age. There were four replicates per treatment and 120 birds in total. At 14 days of age, three chicks from each replicate of each treatment were pooled into a flock and fed commercial broiler diets until 7 weeks of age. Compared to CON group, birds fed with T3-supplemented diets had lower thyroid, abdominal fat pad, gizzard and pancreas weight, and heavier heart weight adjusted for fasted body weight. Chicks with T1.9 had lower ileal densities at 14 day old compared with those in Dp groups or CON. Chicks with T3.8 exhibited greater duodenal and jejunal O2 consumptions as well as ouabain-sensitive O2 consumptions of jejunum and small intestine (duodenum, jejunum, and ileum) by 46.5%, 58.3%, 40.6%, and 26.4% increases, than those in CON. Partial correlation analysis revealed that the weight and length of the small intestine were negatively correlated with body weight gain. Oxygen consumption in the various small intestinal segments was negatively correlated with their respective densities (mg/mm2). In conclusion, a greater oxygen requirement for maintaining ouabain-sensitive respiration (Na+-K+-ATPase) in the intestine limits energy availability to support gastrointestinal tract growth and, thereby, may result in lower body weight gain.","PeriodicalId":10251,"journal":{"name":"Chinese Journal of Physiology","volume":"65 5","pages":"250-257"},"PeriodicalIF":1.8,"publicationDate":"2022-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40456075","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}

引用次数: 0

Exosomes derived from bone marrow mesenchymal stem cells promote proliferation and migration via upregulation yes-associated protein/transcriptional coactivator with PDZ binding motif expression in breast cancer cells. 来自骨髓间充质干细胞的外泌体通过上调乳腺癌细胞中蛋白相关蛋白/ PDZ结合基序的转录共激活因子的表达来促进增殖和迁移。

IF 1.8 4区医学

Chinese Journal of Physiology Pub Date : 2022-09-01 DOI: 10.4103/0304-4920.359800

Wanming Wu, Renfeng Huang, Linyang Ou, Ruiwen Lei

{"title":"Exosomes derived from bone marrow mesenchymal stem cells promote proliferation and migration via upregulation yes-associated protein/transcriptional coactivator with PDZ binding motif expression in breast cancer cells.","authors":"Wanming Wu, Renfeng Huang, Linyang Ou, Ruiwen Lei","doi":"10.4103/0304-4920.359800","DOIUrl":"https://doi.org/10.4103/0304-4920.359800","url":null,"abstract":"Bone marrow mesenchymal stem cells (BM-MSCs), with the properties of self-renewal and pluripotency, can migrate to the tumor sites and exert complex effects on tumor progression and communications by releasing exosomes. However, to our knowledge, only a few studies have reported the effects of BM-MSCs exosomes on breast cancer cells development. Here, utilizing exosomes isolated from in vitro BM-MSCs, we systematically investigated this issue in a breast cancer cell line. In this study, we found that BM-MSCs exosomes are actively incorporated by breast cancer cell MDA-MB-231 cells and subsequently promote MDA-MB-231 cells proliferation and migration. Mechanistically, we further found Yes-associated protein (YAP) and transcriptional coactivator with PDZ binding motif (TAZ) which are Hippo signaling components were involved in this promoting progress. Consistently, YAP and TAZ knockdown could significantly reverse breast cancer cells proliferation and migration improved by BM-MSCs exosomes. Taken together, our findings demonstrated a new mechanism through which BM-MSCs-derived exosomes may contribute to breast cancer cells proliferation and migration, which might provide an evidence for novel drug discovery based on exosomes and Hippo signaling.","PeriodicalId":10251,"journal":{"name":"Chinese Journal of Physiology","volume":"65 5","pages":"233-240"},"PeriodicalIF":1.8,"publicationDate":"2022-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40456073","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}

引用次数: 1

Vitamin C supplementation attenuates oxidative stress and improves erythrocyte deformability in cardiac surgery with cardiopulmonary bypass. 补充维生素C可减轻体外循环心脏手术患者的氧化应激并改善红细胞变形能力。

IF 1.8 4区医学

Chinese Journal of Physiology Pub Date : 2022-09-01 DOI: 10.4103/0304-4920.358234

Ying-Hsuan Tai, Hsiang-Ling Wu, You-Hsiang Chu, Cheng-Hsiung Huang, Shung-Tai Ho, Tso-Chou Lin, Chih-Cherng Lu

{"title":"Vitamin C supplementation attenuates oxidative stress and improves erythrocyte deformability in cardiac surgery with cardiopulmonary bypass.","authors":"Ying-Hsuan Tai, Hsiang-Ling Wu, You-Hsiang Chu, Cheng-Hsiung Huang, Shung-Tai Ho, Tso-Chou Lin, Chih-Cherng Lu","doi":"10.4103/0304-4920.358234","DOIUrl":"https://doi.org/10.4103/0304-4920.358234","url":null,"abstract":"Cardiopulmonary bypass (CPB) depletes endogenous Vitamin C and generates oxidative stress in cardiac surgery. This study aimed to clarify whether Vitamin C supplementation reduces oxidant production and improves erythrocyte deformability in cardiac surgery with CPB. In a randomized and controlled design, 30 eligible patients undergoing cardiac surgery with hypothermic CPB were equally assigned to the Vitamin C group and control group. Subjects of the Vitamin C group and control group received an intravenous infusion of Vitamin C 20 mg·kg-1 and a placebo during rewarming period of CPB, respectively. We measured the plasma level of reactive oxygen species (ROS) and phosphorylation levels of non-muscle myosin IIA (NMIIA) in erythrocyte membrane, as an index of erythrocyte deformability, before and after CPB. Vitamin C supplementation attenuated the surge in plasma ROS after CPB, mean 1.661 ± standard deviation 0.801 folds in the Vitamin C group and 2.743 ± 1.802 in the control group. The tyrosine phosphorylation level of NMIIA after CPB was upregulated in the Vitamin C group compared to the control group, 2.159 ± 0.887 folds and 1.384 ± 0.445 (P = 0.0237). In addition, the phosphorylation of vasodilator-stimulated phosphoprotein (VASP) and focal adhesion kinase (FAK) in erythrocytes was concurrently enhanced in the Vitamin C group after CPB. The phosphorylation level of endothelial nitric oxide synthase in erythrocytes was significantly increased in the Vitamin C group (1.734 ± 0.371 folds) compared to control group (1.102 ± 0.249; P = 0.0061). Patients receiving Vitamin C had lower intraoperative blood loss and higher systemic vascular resistance after CPB compared to controls. Vitamin C supplementation attenuates oxidative stress and improves erythrocyte deformability via VASP/FAK signaling pathway in erythrocytes during CPB.","PeriodicalId":10251,"journal":{"name":"Chinese Journal of Physiology","volume":"65 5","pages":"241-249"},"PeriodicalIF":1.8,"publicationDate":"2022-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40456074","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}

引用次数: 2

Calpain inhibitors inhibit mitochondrial calpain activity to ameliorate apoptosis of cocultured myoblast. 钙蛋白酶抑制剂抑制线粒体钙蛋白酶活性改善共培养成肌细胞凋亡。

IF 1.8 4区医学

Chinese Journal of Physiology Pub Date : 2022-09-01 DOI: 10.4103/0304-4920.359797

Xianliang Zeng, Li Zhao, Zhengliang Chen, Lingjun Kong, Sizeng Chen

{"title":"Calpain inhibitors inhibit mitochondrial calpain activity to ameliorate apoptosis of cocultured myoblast.","authors":"Xianliang Zeng, Li Zhao, Zhengliang Chen, Lingjun Kong, Sizeng Chen","doi":"10.4103/0304-4920.359797","DOIUrl":"https://doi.org/10.4103/0304-4920.359797","url":null,"abstract":"Cancer cachexia is a fatal syndrome associated with muscle regeneration disability. Tumor factors induce the apoptosis of myoblasts to impair the regeneration of skeletal muscle. Cancer cachectic myoblast apoptosis is associated with mitochondria injury. It has been reported that activated mitochondrial calpain caused mitochondria injury in mouse cardiomyocytes and pulmonary smooth muscle. We wondered if mitochondrial calpains exist in skeletal myoblast and their potential role in myoblast apoptosis of cancer cachexia. We used a transwell to build a novel myoblast-carcinoma cell coculture model to simulate the cancer cachexia environment in vitro. Calpain inhibitors, calpastatin (CAST) and calpeptin (CAPT), were used during coculture. We found for the first time that two calpains (calpain-1 and calpain-2) and CAST were present in the mitochondria of myoblast. The activation of mitochondrial calpain decreased mitochondrial complex I activity, promoted mitochondrial permeability transition pore opening, and impaired mitochondrial membrane potential in myoblast during coculture, which induced myoblasts apoptosis. CAST and CAPT protected myoblasts from apoptosis by inhibiting mitochondrial calpain activity, which may attenuate or even reverse cancer cachectic muscle atrophy by improving muscle regeneration ability. Our study provides a new perspective for understanding the mechanism of cancer cachexia, and will further contribute to treat cancer cachexia by focusing on the mitochondrial calpain activity.","PeriodicalId":10251,"journal":{"name":"Chinese Journal of Physiology","volume":"65 5","pages":"226-232"},"PeriodicalIF":1.8,"publicationDate":"2022-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40456072","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}

引用次数: 1