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Effect of Catechins on Myocardial Injury and Inflammatory Factors in Rats with Coronary Heart Disease under PI3K/Akt/eNOS Signaling Pathway |
JIANG Hui-qiong, HONG Yan-ling |
Quanzhou First Hospital, Quanzhou Fujian 362000, China |
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Abstract Objective: To discuss the effect of catechins on myocardial injury and inflammatory factors in rats with coronary heart disease under PI3K/Akt/eNOS signaling pathway. Methods: A total of 50 healthy adult pathogen-free(SPF)-grade SD rats were divided into five groups by random number table method. Except for the blank group, the other four groups were fed with high fat to construct a rat model of coronary artery disease. After the model was successfully constructed, the blank group and the model group were given saline by gavage, the positive group was given 25 mg/kg aspirin by gavage, the low-dose group was given 20 mg/kg catechin by gavage, and the high-dose group was given 60 mg/kg catechin by gavage. The expression levels of PI3K/Akt/eNOS signaling pathway-related proteins, myocardial injury markers, myocardial infarction and myocardial inflammatory factors were observed and compared in the five groups. Results: Overall, there were significant differences in the expression levels of PI3K, p-Akt/Akt, and p-eNOS/eNOS in the five groups of rats(P<0.05); there were significant differences in the expression levels of CK-MB and cTnI in the five groups of rats(P<0.05); there were significant differences in ischemic area, infarct area, and myocardial infarction range in the four groups of rats, except for the blank group(P<0.05); there were significant differences in the expression levels of IL-1β, IL-18, TNF-α, and ET-1 in the five groups of rats(P<0.05). Conclusion: Catechins can reduce the severity of myocardial injury, reduce the range of myocardial infarction, and reduce myocardial inflammation in rats with coronary heart disease by up-regulating expression level of PI3K/Akt/eNOS signaling pathway-related proteins. Compared with aspirin, high-dose catechins have a more prominent protective effect on the myocardium of rats with coronary heart disease.
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Received: 15 February 2024
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Corresponding Authors:
HONG Yan-ling. E-mail: 454028590@qq.com
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[1] Chinese Medical Association, Chinese Medical Journals Publishing House Co., Ltd, Chinese Society of General Practice, et al. Guideline for primary care of stable coronary artery disease(2020)[J].Chinese Journal of General Practitioners, 2021, 20(3): 265-273. [2] Khan MA, Hashim MJ, Mustafa H, et al.Global epidemiology of ischemic heart disease: Results from the global burden of disease study[J]. Cureus, 2020, 12(7): e9349. [3] Muscella A, Stefàno E, Marsigliante S.The effects of exercise training on lipid metabolism and coronary heart disease[J]. Am J Physiol Heart Circ Physiol, 2020, 319(1): H76-H88. [4] Cai S, Zhao M, Zhou B, et al.Mitochondrial dysfunction in macrophages promotes inflammation and suppresses repair after myocardial infarction[J]. J Clin Invest, 2023, 133(4): e159498. [5] Zhang Wen, Song Junke, Zhu Xiaoyu, et al.Effect of epigallocatechin on reducing LPS-induced BV2 cell inflammatory response through TLR4/MyD88/NF-κB signaling pathway[J].Herald of Medicine, 2020, 39(6): 735-740. [6] Zhou Hui, Lei Yuhua, Zhang Fugui, et al.Mechanism of catechin on endothelial function in aged rats with coronary heart disease based on MEK/ERK signaling pathway[J]. Chinese Journal of Difficult and Complicated Cases, 2021, 20(4): 353-357. [7] Bai J, Wang Q, Qi J, et al.Promoting effect of baicalin on nitric oxide production in CMECs via activating the PI3K-AKT-eNOS pathway attenuates myocardial ischemia-reperfusion injury[J]. Phytomedicine, 2019, 63: 153035. [8] He F, Xu BL, Chen C, et al.Methylophiopogonanone A suppresses ischemia/reperfusion-induced myocardial apoptosis in mice via activating PI3K/Akt/eNOS signaling pathway[J]. Acta Pharmacol Sin, 2016, 37(6): 763-771. [9] Ashall V, Morton D, Clutton E.A declaration of Helsinki for animals[J]. Vet Anaesth Analg, 2023, 50(4): 309-314. [10] Tie G, Yan J, Yang Y, et al.Oxidized low-density lipoprotein induces apoptosis in endothelial progenitor cells by inactivating the phosphoinositide 3-kinase/Akt pathway[J]. J Vasc Res, 2010, 47(6): 519-530. [11] Kuzkaya N, Weissmann N, Harrison DG, et al.Interactions of peroxynitrite, tetrahydrobiopterin, ascorbic acid, and thiols: implications for uncoupling endothelial nitric-oxide synthase[J]. J Biol Chem, 2003, 278(25): 22546-22554. [12] Bernatoniene J, Kopustinskiene DM.The role of catechins in cellular responses to oxidative stress[J]. Molecules, 2018, 23(4): 965. [13] Wu Simin, Yuan Mei, Gao Ziqi, et al.Development of epigallocatechin gallate in the inflammatory response of skin photoaging[J]. Journal of Food Safety&Quality,2021,12(7): 2513-2519. |
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