RV01 is a novel quinoline-substituted analogue of resveratrol that inhibits DNA damage, reduces ethanol-induced acetaldehyde dehydrogenase (ALDH2) mRNA expression, and has hydroxyl radical scavenging activity. rV01 reduces iNOS expression and has anti-neuroinflammatory effects. rV01 reduces tumor necrosis factor-a (TNF-a) and interleukin-6 (IL-6) mRNA levels and secretion. RV01 reduced tumor necrosis factor-a (TNF-a) and interleukin-6 (IL-6) mRNA levels and secretion, inhibited lps-induced ROS production and nicotinamide adenine dinucleotide phosphate (NADPH) oxidase activation, decreased toll-like receptor 4 (TLR4) protein expression, and inhibited lps-induced activation of mitogen-activated protein kinase (MAPK) and nuclear transcription factor-кB (NF-кB) signaling pathways.

一种新颖的喹啉基取代白藜芦醇类似物(RV01)对脂多糖(LPS)诱导的小胶质细胞活化的抗神经炎症效应及其潜在机制进行了研究。通过MTT检测细胞活力，通过亚硝酸盐检测来确定一氧化氮(NO)释放。采用DPPH还原实验和DCFH-DA实验确定自由基清除活性和活性氧(ROS)产生。RV01 (1-30 µm) 预处理显著减少了LPS (1 µg mL^-1) 刺激后的NO释放和一氧化氮合酶(iNOS)表达，并未观察到明显的细胞毒性。RV01降低了肿瘤坏死因子α(TNF-α)和白细胞介素-6 (IL-6)的mRNA水平和分泌。此外，RV01抑制了LPS诱导的ROS产生和烟酰胺腺嘌呤二核苷酸(NADPH)氧化酶激活，并减少了Toll样受体4 (TLR4)的蛋白表达，并阻止了LPS诱导的丝裂原活化蛋白激酶(MAPK)和核转录因子-κB (NF-κB)信号通路的活化。此外，与LPS和RV01共同处理的小胶质细胞的条件培养基能缓解由活化N9小胶质细胞的条件培养基诱导的SH-SY5Y细胞死亡。最后，进一步通过小鼠神经炎症模型证实了RV01在体内的效果。研究结果显示RV01抑制了小胶质细胞介导的神经炎症，并保护神经元免受炎症损伤。[2]