Zhou Man-Yu, Liu Bing-Qing, Gao Xin, Zhang Shu-Jing, Jiang Yang, Yang Tao, Sun Jian-Bin, Zhang Xi, Liao Yan
School of Traditional Chinese Medicine, Beijing University of Chinese Medicine, Beijing 102446, China.
Chongqing Academy of Chinese Materia Medica, Chongqing 400065, China.
Int J Biol Macromol. 2025 Apr;300:140270. doi: 10.1016/j.ijbiomac.2025.140270. Epub 2025 Jan 23.
Age-related cataract (ARC) remains the leading cause of blindness worldwide. Sagittaria sagittifolia polysaccharide (SSP) extract, a key component of Sagittaria sagittifolia L., exhibits anti-oxidant and anti-apoptotic effects with potential applications in ARC. This study aimed to explore the therapeutic potential of SSP in ARC and the underlying mechanisms. In sodium selenite-induced cataracts in rats and hydrogen peroxide (HO)-induced human lens epithelial B3 (HLEB3) cells, SSP significantly improved lens opacity and pathological changes and alleviated apoptosis and endoplasmic reticulum stress (ERS)-related injury indicators (by inhibiting the intracellular Ca and protein expression of Bcl-2-associated X, cleaved caspase-3, binding immunoglobulin heavy chain protein, protein kinase RNA-like kinase, inositol-requiring enzyme 1α, activating transcription factor 6, C/EBP homology protein, c-Jun N terminal kinase, caspase-12, and calpain-2). In addition, SSP increased the expression of nuclear factor erythroid 2-related factor 2 (Nrf2), heme oxygenase-1, sarco/endoplasmic reticulum-type calcium transport ATPase 2, and B-cell lymphoma-2. After applying Nrf2 knockdown technology by transferring short interfering RNA in HLEB3 cells, SSP demonstrated its protective role by activating Nrf2 and inhibiting ERS-mediated apoptosis. These findings indicate that SSP may protect against ARC by regulating Nrf2/ERS-mediated apoptosis, providing potential evidence for its use in preventing or delaying ARC.
年龄相关性白内障（ARC）仍然是全球失明的主要原因。慈姑多糖（SSP）提取物是慈姑的关键成分，具有抗氧化和抗凋亡作用，在ARC中具有潜在应用价值。本研究旨在探讨SSP在ARC中的治疗潜力及其潜在机制。在亚硒酸钠诱导的大鼠白内障和过氧化氢（H₂O₂）诱导的人晶状体上皮B3（HLEB3）细胞中，SSP显著改善晶状体混浊和病理变化，减轻凋亡和内质网应激（ERS）相关损伤指标（通过抑制细胞内Ca²⁺以及Bcl-2相关X蛋白、裂解的半胱天冬酶-3、结合免疫球蛋白重链蛋白、蛋白激酶RNA样激酶、肌醇需求酶1α、活化转录因子6、C/EBP同源蛋白、c-Jun N末端激酶、半胱天冬酶-12和钙蛋白酶-2的蛋白表达）。此外，SSP增加了核因子红细胞2相关因子2（Nrf2）、血红素加氧酶-1、肌浆/内质网型钙转运ATP酶2和B细胞淋巴瘤-2的表达。在HLEB3细胞中通过转染小干扰RNA应用Nrf2敲低技术后，SSP通过激活Nrf2和抑制ERS介导的凋亡发挥其保护作用。这些发现表明，SSP可能通过调节Nrf2/ERS介导的凋亡来预防ARC，为其用于预防或延缓ARC提供了潜在证据。
