Wang Wei, Gao Jia, Mu Qianqian, Zhang Dan, Yang Fen, Cheng Wubo
Opthalmology, Kunming Municipal Hospital of Traditional Chinese Medicine, Kunming, China.
Chengdu University of Traditional Chinese Medicine, Chengdu, China.
Medicine (Baltimore). 2025 Jan 10;104(2):e41257. doi: 10.1097/MD.0000000000041257.
Bushen-Huoxue-Mingmu-Formula (MMF) has achieved definite clinical efficacy. However, its mechanism is still unclear.
Investigating the molecular mechanism of MMF to protect retinal ganglion cells (RGCs).
This study developed a pressurization-induced model of damaged RGCs, which were then treated with a serum supplemented with MMF. The effects of MMF on proliferation, apoptosis, adenosine 5'-triphosphate content, and mitochondrial structure of RGCs were investigated, and the underlying molecular mechanism was explored by RNA interference experiment.
In the pressurization-induced RGC injury model, apoptosis rate increased, cell proliferation decreased, adenosine 5'-triphosphate content reduced, mitochondrial structure was disrupted, BCL2-associated X, cleaved caspase-3, and microtubule-associated proteins light chain 3 II/I protein expression enhanced, B cell lymphoma-2 and p62 protein expression decreased, and the Pink1/Parkin pathway was activated. The stress-induced damage to RGCs was, however, reversible following MMF-mediated inhibition of the Pink1/Parkin pathway. Pink1 short-hairpin RNA downregulated Pink1 expression in RGCs, which led to outcomes that aligned with those observed with MMF intervention.
MMF altered the expression of apoptosis- and autophagy-related proteins and possibly inhibited the Pink1/Parkin signaling pathway, which led to reduced pressurization-induced mitochondrial autophagy in RGCs. This preventive effect of MMF on RGCs can be potentially useful to preserve the viability of RGCs.
补肾活血明目方(MMF)已取得确切的临床疗效。然而,其作用机制仍不清楚。
探讨MMF保护视网膜神经节细胞(RGCs)的分子机制。
本研究建立了压力诱导的RGCs损伤模型,然后用含MMF的血清对其进行处理。研究MMF对RGCs增殖、凋亡、三磷酸腺苷含量及线粒体结构的影响,并通过RNA干扰实验探索其潜在的分子机制。
在压力诱导的RGC损伤模型中,细胞凋亡率升高,细胞增殖减少,三磷酸腺苷含量降低,线粒体结构破坏,BCL2相关X蛋白、裂解的半胱天冬酶-3和微管相关蛋白轻链3 II/I蛋白表达增强,B细胞淋巴瘤-2和p62蛋白表达降低,Pink1/Parkin通路被激活。然而,MMF介导的Pink1/Parkin通路抑制可使压力诱导的RGCs损伤得到逆转。Pink1短发夹RNA下调了RGCs中Pink1的表达,其导致的结果与MMF干预所观察到的结果一致。
MMF改变了凋亡和自噬相关蛋白的表达,并可能抑制了Pink1/Parkin信号通路,从而减少了压力诱导的RGCs线粒体自噬。MMF对RGCs的这种保护作用可能有助于维持RGCs的活力。