Azilsartan prevents muscle loss and fast- to slow-twitch muscle fiber shift in natural ageing sarcopenic rats.

IF 1.7 4区医学 Q3 PHARMACOLOGY & PHARMACY

Canadian journal of physiology and pharmacology Pub Date : 2024-05-01 Epub Date: 2023-12-20 DOI:10.1139/cjpp-2023-0265

Priyanka Prajapati, Anand Kumar, Shubhada Mangrulkar, D R Chaple, Shubhini A Saraf, Sapana Kushwaha

{"title":"Azilsartan prevents muscle loss and fast- to slow-twitch muscle fiber shift in natural ageing sarcopenic rats.","authors":"Priyanka Prajapati, Anand Kumar, Shubhada Mangrulkar, D R Chaple, Shubhini A Saraf, Sapana Kushwaha","doi":"10.1139/cjpp-2023-0265","DOIUrl":null,"url":null,"abstract":"<p><p>Sarcopenia is a musculoskeletal disease that reduces muscle mass and strength in older individuals. The study investigates the effects of azilsartan (AZL) on skeletal muscle loss in natural sarcopenic rats. Male Sprague-Dawley rats aged 4-6 months and 18-21 months were selected as young-matched control and natural-aged (sarcopenic) rats, respectively. Rats were allocated into young and old control (YC and OC) and young and old AZL treatment (YT and OT) groups, which received vehicles and AZL (8 mg/kg, orally) for 6 weeks. Rats were then sacrificed after muscle function analysis. Serum and gastrocnemius (GN) muscles were isolated for further endpoints. AZL significantly improved muscle grip strength and antioxidant levels in sarcopenic rats. AZL also restored the levels of insulin, testosterone, and muscle biomarkers such as myostatin and creatinine kinase in sarcopenic rats. Furthermore, AZL treatment improved the cellular and ultrastructure of GN muscle and prevented the shift of type II (glycolytic) myofibers to type I (oxidative) myofibers. The results showed that AZL intervention restored protein synthesis in natural sarcopenic rats by increasing p-Akt-1 and decreasing muscle RING-finger protein-1 and tumor necrosis factor alpha immunoexpressions. In conclusion, the present findings showed that AZL could be an effective intervention in treating age-related muscle impairments.</p>","PeriodicalId":9520,"journal":{"name":"Canadian journal of physiology and pharmacology","volume":" ","pages":"342-360"},"PeriodicalIF":1.7000,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Canadian journal of physiology and pharmacology","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1139/cjpp-2023-0265","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2023/12/20 0:00:00","PubModel":"Epub","JCR":"Q3","JCRName":"PHARMACOLOGY & PHARMACY","Score":null,"Total":0}

引用次数: 0

Abstract

Sarcopenia is a musculoskeletal disease that reduces muscle mass and strength in older individuals. The study investigates the effects of azilsartan (AZL) on skeletal muscle loss in natural sarcopenic rats. Male Sprague-Dawley rats aged 4-6 months and 18-21 months were selected as young-matched control and natural-aged (sarcopenic) rats, respectively. Rats were allocated into young and old control (YC and OC) and young and old AZL treatment (YT and OT) groups, which received vehicles and AZL (8 mg/kg, orally) for 6 weeks. Rats were then sacrificed after muscle function analysis. Serum and gastrocnemius (GN) muscles were isolated for further endpoints. AZL significantly improved muscle grip strength and antioxidant levels in sarcopenic rats. AZL also restored the levels of insulin, testosterone, and muscle biomarkers such as myostatin and creatinine kinase in sarcopenic rats. Furthermore, AZL treatment improved the cellular and ultrastructure of GN muscle and prevented the shift of type II (glycolytic) myofibers to type I (oxidative) myofibers. The results showed that AZL intervention restored protein synthesis in natural sarcopenic rats by increasing p-Akt-1 and decreasing muscle RING-finger protein-1 and tumor necrosis factor alpha immunoexpressions. In conclusion, the present findings showed that AZL could be an effective intervention in treating age-related muscle impairments.

查看原文本刊更多论文

阿齐沙坦能防止自然衰老型肌肉疏松大鼠的肌肉损失和快慢肌肌纤维转变

肌肉疏松症是一种肌肉骨骼疾病，会降低老年人的肌肉质量和力量。本研究调查了阿齐沙坦（AZL）对自然肌少症大鼠骨骼肌损失的影响。研究人员选择了年龄分别为 4-6 个月和 18-21 个月的雄性 Sprague-Dawley 大鼠作为年轻对照组和自然年龄组（肌肉疏松）大鼠。大鼠被分为年轻组和老年对照组（YC 和 OC）以及年轻组和老年 AZL 治疗组（YT 和 OT），分别接受药物和阿齐沙坦（8 毫克/千克，口服）治疗六周。大鼠在肌肉功能分析后被处死。血清和腓肠肌（GN）肌肉被分离出来，用于进一步的终点检测。AZL 能明显改善肌肉疏松大鼠的肌肉握力和抗氧化水平。AZL 还能恢复肌肉疏松大鼠的胰岛素、睾酮和肌肉生物标志物（如肌促蛋白和肌酸激酶）水平。此外，AZL 治疗还改善了 GN 肌肉的细胞和超微结构，防止了 II 型（糖酵解）肌纤维向 I 型（氧化）肌纤维的转变。结果表明，AZL干预通过增加p-Akt-1和降低MuRF-1和TNF-α免疫表达，恢复了天然肌肉疏松大鼠的蛋白质合成。总之，本研究结果表明，AZL 是治疗与年龄有关的肌肉损伤的有效干预措施。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

求助全文

约1分钟内获得全文求助全文

来源期刊

Canadian journal of physiology and pharmacology 医学-生理学

CiteScore

4.00

自引率

4.80%

发文量

审稿时长

3-8 weeks

期刊介绍： Published since 1929, the Canadian Journal of Physiology and Pharmacology is a monthly journal that reports current research in all aspects of physiology, nutrition, pharmacology, and toxicology, contributed by recognized experts and scientists. It publishes symposium reviews and award lectures and occasionally dedicates entire issues or portions of issues to subjects of special interest to its international readership. The journal periodically publishes a “Made In Canada” special section that features invited review articles from internationally recognized scientists who have received some of their training in Canada.