卡托普利抑制硫代乙酰胺诱导的大鼠肝毒性中哺乳动物雷帕霉素靶细胞信号和炎症及氧化应激生物标志物。
Captopril suppresses hepatic mammalian target of rapamycin cell signaling and biomarkers of inflammation and oxidative stress in thioacetamide-induced hepatotoxicity in rats.
机构信息
Department of Physiology, College of Medicine, King Khalid University, Abha, Saudi Arabia.
Department of Medicine, College of Medicine, King Khalid University, Abha, Saudi Arabia.
出版信息
Arch Physiol Biochem. 2021 Oct;127(5):414-421. doi: 10.1080/13813455.2019.1647249. Epub 2019 Jul 31.
BACKGROUND
The potential inhibitory effects of captopril, the angiotensin-converting enzyme inhibitor, on thioacetamide (TAA)-induced hepatic mammalian target of rapamycin (mTOR), liver injury enzymes, blood pressure, and biomarkers of inflammation and oxidative stress have not been investigated before.
MATERIALS AND METHODS
Rats were either injected with TAA (200 mg/kg; twice a week for 8 weeks) before being sacrificed after 10 weeks (model group) or were pretreated with captopril (150 mg/kg) daily for two weeks prior to TAA injections and continued receiving both agents until the end of the experiment (protective group).
RESULTS
Captopril significantly ( < .05) inhibited TAA-induced hypertension, liver tissue levels of mTOR, TIMP-1, TNF-α, IL-6, MDA; and blood levels of lipids, ALT, and AST. We further demonstrated a significant ( < .01) positive correlation between mTOR scoring and the levels of inflammatory, oxidative and liver injury biomarkers.
CONCLUSIONS
Captopril protects against TAA-induced mTOR, liver injury enzymes, dyslipidemia, hypertension, inflammation, and oxidative stress.
背景
血管紧张素转换酶抑制剂卡托普利对硫代乙酰胺（TAA）诱导的肝哺乳动物雷帕霉素靶蛋白（mTOR）、肝损伤酶、血压以及炎症和氧化应激生物标志物的潜在抑制作用尚未被研究过。
材料与方法
大鼠先接受 TAA（200mg/kg；每周两次，共 8 周）注射，然后在 10 周后被处死（模型组），或者在 TAA 注射前用卡托普利（150mg/kg）预处理两周，并在实验结束前继续同时给予两种药物（保护组）。
结果
卡托普利显著（<0.05）抑制了 TAA 诱导的高血压、肝组织 mTOR、TIMP-1、TNF-α、IL-6、MDA 水平以及血液中脂质、ALT 和 AST 水平。我们进一步证明了 mTOR 评分与炎症、氧化和肝损伤生物标志物水平之间存在显著（<0.01）的正相关关系。
结论
卡托普利可预防 TAA 诱导的 mTOR、肝损伤酶、血脂异常、高血压、炎症和氧化应激。
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