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白皮松酸对糖尿病大鼠的心脏保护作用:可能的 PPAR-γ 通路机制。

The Cardioprotective Effect of Corosolic Acid in the Diabetic Rats: A Possible Mechanism of the PPAR-γ Pathway.

机构信息

Department of Pharmacology, College of Pharmacy, Prince Sattam Bin Abdulaziz University, Al Kharj 11942, Saudi Arabia.

Chitkara College of Pharmacy, Chitkara University, Rajpura 140401, Punjab, India.

出版信息

Molecules. 2023 Jan 17;28(3):929. doi: 10.3390/molecules28030929.

Abstract

The study was conducted to determine whether corosolic acid could protect the myocardium of diabetic rats from damage caused by isoproterenol (ISO) and, if so, how peroxisome proliferator-activated receptor gamma (PPAR-γ) activation might contribute into this protection. Diabetes in the rats was induced by streptozotocin (STZ), and it was divided into four groups: the diabetic control group, diabetic rats treated with corosolic acid, diabetic rats treated with GW9662, and diabetic rats treated with corosolic acid plus GW9662. The study was carried out for 28 days. The diabetic control and ISO control groups showed a decrease in mean arterial pressure (MAP) and diastolic arterial pressure (DAP) and an increase in systolic arterial pressure (SAP). The rat myocardium was activated by corosolic acid treatment, which elevated PPAR-γ expression. A histopathological analysis showed a significant reduction in myocardial damage by reducing myonecrosis and edema. It was found that myocardial levels of CK-MB and LDH levels were significantly increased after treatment with corosolic acid. By decreasing lipid peroxidation and increasing endogenous antioxidant levels, corosolic acid therapy showed a significant improvement over the ISO diabetic group. In conclusion, our results prove that corosolic acid can ameliorate ISO-induced acute myocardial injury in rats. Based on these results, corosolic acid seems to be a viable new target for the treatment of cardiovascular diseases and other diseases of a similar nature.

摘要

本研究旨在探讨熊果酸是否能保护糖尿病大鼠心肌免受异丙肾上腺素(ISO)的损伤,如果可以,过氧化物酶体增殖物激活受体γ(PPAR-γ)的激活是如何促成这种保护作用的。大鼠糖尿病通过链脲佐菌素(STZ)诱导,并分为四组:糖尿病对照组、糖尿病大鼠熊果酸组、糖尿病大鼠 GW9662 组和糖尿病大鼠熊果酸加 GW9662 组。研究进行了 28 天。糖尿病对照组和 ISO 对照组的平均动脉压(MAP)和舒张压(DAP)下降,收缩压(SAP)升高。熊果酸处理激活了大鼠心肌,增加了 PPAR-γ 的表达。组织病理学分析显示,通过减少肌坏死和水肿,心肌损伤显著减少。结果发现,用熊果酸处理后,心肌肌酸激酶同工酶(CK-MB)和乳酸脱氢酶(LDH)水平显著升高。熊果酸治疗通过降低脂质过氧化和增加内源性抗氧化水平,与 ISO 糖尿病组相比有显著改善。总之,我们的研究结果证明熊果酸可以改善 ISO 诱导的大鼠急性心肌损伤。基于这些结果,熊果酸似乎是治疗心血管疾病和其他类似性质疾病的一个有前途的新靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/df8d/9919720/1b1f063925b1/molecules-28-00929-sch001.jpg

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