Green Tea (Camellia sinensis) Extract Increased Topoisomerase IIβ, Improved Antioxidant Defense, and Attenuated Cardiac Remodeling in an Acute Doxorubicin Toxicity Model

Abstract

Experimental studies have shown the action of green tea in modulating cardiac remodeling. However, the effects of green tea on the cardiac remodeling process induced by doxorubicin (DOX) are not known. Therefore, this study is aimed at evaluating whether green tea extract could attenuate DOX-induced cardiac remodeling, assessed by cardiac morphological and functional changes and associated with the evaluation of different modulators of cardiac remodeling. The animals were divided into four groups: the control group (C), the green tea group (GT), the DOX group (D), and the DOX and green tea group (DGT). Groups C and GT received intraperitoneal sterile saline injections, D and DGT received intraperitoneal injections of DOX, and GT and DGT were fed chow supplemented with green tea extract for 35 days prior to DOX injection. After forty-eight hours, we performed an echocardiogram and euthanasia and collected the materials for analysis. Green tea attenuated DOX-induced cardiotoxicity by increasing cardiac function and decreasing the concentric remodeling. Treatment with DOX increased oxidative stress in the heart, marked by a higher level of lipid hydroperoxide (LH) and lower levels of antioxidant enzymes. Treatment with green tea increased the antioxidant enzymes’ activity and decreased the production of LH. Green tea extract increased the expression of Top2-β independent of DOX treatment. The activity of ATP synthase, citrate synthase, and complexes I and II decreased with DOX, without the effects of green tea. Both groups that received DOX presented with a lower ratio of P-akt/T-akt and a higher expression of CD45, TNFα, and intermediate MMP-2, without the effects of green tea. In conclusion, green tea attenuated cardiac remodeling induced by DOX and was associated with increasing the expression of Top2-β and lowering oxidative stress. However, energy metabolism and inflammation probably do not receive the benefits induced by green tea in this model.

Leaf extracts from Camellia sinensis and Argania spinosa suppress oxidative stress and chemokine release in human 3-dimensional cultured epidermis exposed to PM2.5 collected with cyclonic separation

“…Xiang et al (2016) reported the suppressive effects of Camellia sinensis on breast cancer. Camellia sinensis extract was reported to attenuate cardiac remodeling accompanied by acute doxorubicin toxicity (Modesto et al, 2021) and suppress brain ischemic injury induced by middle cerebral artery occlusion (Machin et al, 2021).…”

Supplementation with Two New Standardized Tea Extracts Prevents the Development of Hypertension in Mice with Metabolic Syndrome

“…Likewise, pretreatment with a green tea extract administered before regional myocardial ischemia-reperfusion improved myocardial contractility through the attenuation of calcium overload in rats [ 45 ]. The beneficial effects of tea on cardiac function are the result, at least in part, of the presence of polyphenols which are reported to exert antioxidant effects in the heart both in vivo [ 46 , 47 ] and in vitro [ 48 , 49 , 50 ]. However, in this study we did not find differences in the gene expression of antioxidant enzymes among the experimental groups.…”

Cardioprotective Effects of Aconite in Isoproterenol-Induced Myocardial Infarction in Rats

“…MDA, a major metabolite of oxidative free radicals, reflects the degree of peroxidation of myocardial tissue. And SOD as a vital antioxidant enzyme can improve myocardial oxidative stress injury by scavenging oxygen free radicals [ 6 , 37 ]. AEBA significantly decreased the content of MDA and increased the serum SOD activity, which might contribute to its effects on alleviating the injury degree of inflammation and fibrosis of the heart tissue in ISO-induced MI rats.…”

“…It is well recognized that oxidative stress, caused by the imbalance between the scavenging and production of oxygen radicals, aggravates maladaptive left ventricular remodeling [ 5 ]. Superoxide dismutase (SOD), an important antioxidant enzyme, is decreased in MI [ 6 ]. Additionally, oxidative stress is associated with inflammatory responses in the infarcted heart, manifested by the infiltration of inflammatory cells (such as macrophages), secretion of proinflammatory mediators [ 7 ], and activation of the inflammatory cascades [ 8 ], resulting in exacerbating abnormal vascular remodeling and cardiac dysfunction [ 9 , 10 ].…”