Poasakate Anuson, Maneesai Putcharawipa, Rattanakanokchai Siwayu, Bunbupha Sarawoot, Tong-Un Terdthai, Pakdeechote Poungrat
Department of Physiology, Faculty of Medicine, Khon Kaen University, Khon Kaen 40002, Thailand.
Faculty of Veterinary Medicine, Khon Kaen University, Khon Kaen 40002, Thailand.
Antioxidants (Basel). 2021 Feb 4;10(2):237. doi: 10.3390/antiox10020237.
Genistein is an isoflavone found in soybeans. This study evaluates the protective effects of genistein on N-nitro-L-arginine methyl ester hydrochloride (L-NAME)-induced hypertension, cardiac remodeling, and dysfunction in rats. Male Wistar rats were treated with L-NAME 40 mg/kg/day together for 5 weeks, with or without genistein at a dose of 40 or 80 mg/kg/day or lisinopril 5 mg/kg/day ( = 8 per group). Genistein prevented L-NAME-induced hypertension in rats. Increases in the left ventricular weight, metalloproteinase-2, metalloproteinase-9, and collagen type I intensity were observed in L-NAME rats, and these changes were attenuated in the genistein-treated group. Genistein reduced circulating angiotensin-converting enzyme activity and angiotensin II concentrations in L-NAME rats. L-NAME increased plasma and cardiac malondialdehyde and vascular superoxide generations, as well as reductions of serum and cardiac catalase activities in rats. Plasma nitrate/nitrite were protected in the genistein-treated group. Genistein prevented the L-NAME-induced overexpression of angiotensin II receptor type I (ATR), nicotinamide adenine dinucleotide phosphate (NADPH) oxidase subunit 2 (gp91), and transforming growth factor beta I (TGF-β1) in hypertensive rats. In conclusion, genistein exhibited a cardioprotective effect in hypertensive rats in this study. The molecular mechanisms might be mediated by suppression of oxidative stress through the Ang II/ATR/NADPH oxidase/TGF-β1 signaling pathway.
染料木黄酮是一种存在于大豆中的异黄酮。本研究评估了染料木黄酮对N-硝基-L-精氨酸甲酯盐酸盐（L-NAME）诱导的大鼠高血压、心脏重塑和功能障碍的保护作用。雄性Wistar大鼠连续5周每天接受40 mg/kg的L-NAME治疗，同时分别给予40或80 mg/kg/天的染料木黄酮或5 mg/kg/天的赖诺普利（每组n = 8）。染料木黄酮可预防L-NAME诱导的大鼠高血压。L-NAME处理的大鼠左心室重量、金属蛋白酶-2、金属蛋白酶-9和I型胶原强度增加，而在染料木黄酮处理组中这些变化减弱。染料木黄酮降低了L-NAME处理大鼠的循环血管紧张素转换酶活性和血管紧张素II浓度。L-NAME增加了大鼠血浆和心脏中的丙二醛含量以及血管超氧化物的生成，同时降低了血清和心脏中的过氧化氢酶活性。染料木黄酮处理组的血浆硝酸盐/亚硝酸盐水平得到了保护。染料木黄酮可预防L-NAME诱导的高血压大鼠中血管紧张素II 1型受体（ATR）、烟酰胺腺嘌呤二核苷酸磷酸（NADPH）氧化酶亚基2（gp91）和转化生长因子β1（TGF-β1）的过度表达。总之，本研究中染料木黄酮在高血压大鼠中表现出心脏保护作用。其分子机制可能是通过Ang II/ATR/NADPH氧化酶/TGF-β1信号通路抑制氧化应激来介导的。
