Translational Nanomedicine and Lifestyle Disease Research Laboratory, Department of Biochemistry, University of Kerala, Kariavattom campus, Thiruvananthapuram, 695034, Kerala, India.
Centre for Advanced Cancer Research, Department of Biochemistry, University of Kerala, Kariavattom campus, Thiruvananthapuram, 695034, Kerala, India.
Cell Biochem Biophys. 2024 Dec;82(4):3681-3694. doi: 10.1007/s12013-024-01456-w. Epub 2024 Aug 2.
Robinin is one of the glycosyloxyflavones that has been less explored for its therapeutic application, especially in the field of CVD. Herein, we explored the cardioprotective efficacy of Robinin by using HO and Doxorubicin (DOX) - treated H9c2 cells as an in vitro model. HO and DOX treatment resulted in severe cellular damage to the cardiomyocytes, which was followed by apoptosis. Apoptosis and nuclear morphology were analysed through Hoechst 33342 and AO/EB staining. qPCR was employed to detect the expression of apoptosis as well as ERS-related markers. Reactive oxygen species (ROS) generation was observed using DCFH-DA staining and FACS analysis. Signaling pathways involved were analysed using Western blot. Robinin pre-treatment considerably decreased the apoptotic rate by boosting the endogenous anti-oxidative activity and lowering the activity of Malonaldehyde and Lactate dehydrogenase enzyme. Robinin also inhibited the generation of ROS. Robinin reduced the expression of ERS-associated genes and proteins, thereby decreasing apoptosis-related proteins. Upon comparing the cardioprotective effect of Robinin with a known cardioprotective agent Dexrazoxane (DEX) it was revealed that DEX has more cardioprotective effect against DOX than HO-induced stress, while Robinin showed a significant protective effect against both HO and DOX induced stress.
罗比宁是一种糖苷氧基黄酮，其治疗应用，尤其是在心血管疾病领域的研究较少。在此，我们通过使用 H9c2 细胞作为体外模型，探讨了罗比宁的心脏保护作用。HO 和 DOX 处理导致心肌细胞严重损伤，随后发生细胞凋亡。通过 Hoechst 33342 和 AO/EB 染色分析细胞凋亡和核形态。通过 qPCR 检测凋亡以及 ERS 相关标志物的表达。通过 DCFH-DA 染色和 FACS 分析观察活性氧 (ROS) 的产生。使用 Western blot 分析涉及的信号通路。罗比宁预处理通过增强内源性抗氧化活性和降低丙二醛和乳酸脱氢酶的活性，显著降低了细胞凋亡率。罗比宁还抑制了 ROS 的产生。罗比宁降低了与 ERS 相关的基因和蛋白的表达，从而降低了与凋亡相关的蛋白。将罗比宁的心脏保护作用与已知的心脏保护剂右雷佐生 (DEX) 进行比较后发现，DEX 对 DOX 的心脏保护作用强于 HO 诱导的应激，而罗比宁对 HO 和 DOX 诱导的应激均显示出显著的保护作用。
