Department of Physiology, Baicheng Medical College, Baicheng, 137000 Jilin, China.
Department of Physiology and Pathophysiology, College of Medicine, Yanbian University, Yanji, 133000 Jilin, China.
Dis Markers. 2022 Aug 21;2022:4688203. doi: 10.1155/2022/4688203. eCollection 2022.
To explore the impact of genistein (Gen) on the apoptosis of neuronal cells in naturally aged rats and its mechanism.
Fifty SD male rats were allocated into five groups at random, including youth group (3M group), natural aging group (24M group), and Gen low-, medium-, and high-dose groups. Starting from 18 months of age, Gen 10, 30, and 60 mg-kg were administered via gavage to the Gen low-, medium-, and high-dose groups, respectively, while the rats in the natural aging group was given saline by gavage until 24 months of age, and the drug was stopped for 1 d per week for 6 months. The protein expression of target genes was examined using western blotting.
In contrast to the 3M group, the 24M group rats showed disturbed neuronal cell arrangement and massive cell degeneration. After 6 months of Gen intervention, in contrast to the 24M group, the neural cell pathology in the CA3 area of the hippocampus improved and cell apoptotic decreased observably. In contrast to the 3M group, the protein expression of c-Jun amino-terminal kinase (p-JNK), C/EBP homologous protein (CHOP), inflammatory vesicle 3-associated factor (NLRP3), cysteine protease-1 (Caspase-1), and apoptosis-related punctate protein (ASC) and downstream inflammatory factors in the hippocampus was obviously increased in the 24M group. In contrast to the 24M group, the protein expression of p-JNK, CHOP, NLRP3, Caspase-1, and ASC and downstream inflammatory factors in the hippocampus was observably declined in Gen groups.
Gen has a protective effect on hippocampal neurons in aging rat brain tissue via the inhibition of the ERS apoptotic signaling pathway and NLRP3 inflammatory vesicle activation.
探讨染料木黄酮（Gen）对自然衰老大鼠神经元细胞凋亡的影响及其机制。
将 50 只雄性 SD 大鼠随机分为 5 组，包括青年组（3M 组）、自然衰老组（24M 组）和低、中、高剂量 Gen 组。自 18 个月龄开始，分别给予低、中、高剂量 Gen 组 10、30 和 60mg/kg Gen 灌胃，自然衰老组给予生理盐水灌胃，直至 24 个月龄，每周停药 1 天，共 6 个月。采用 Western blot 法检测靶基因蛋白表达。
与 3M 组相比，24M 组大鼠神经元细胞排列紊乱，细胞大量变性。经过 6 个月的 Gen 干预后，与 24M 组相比，海马 CA3 区神经细胞病理明显改善，细胞凋亡明显减少。与 3M 组相比，24M 组大鼠海马组织中 c-Jun 氨基末端激酶（p-JNK）、C/EBP 同源蛋白（CHOP）、炎症小体 3 相关因子（NLRP3）、半胱氨酸蛋白酶-1（Caspase-1）和凋亡相关斑点蛋白（ASC）及下游炎症因子的蛋白表达明显增加，而 Gen 组大鼠海马组织中 p-JNK、CHOP、NLRP3、Caspase-1 和 ASC 及下游炎症因子的蛋白表达明显下降。
Gen 通过抑制 ERS 凋亡信号通路和 NLRP3 炎症小体的激活，对衰老大鼠脑组织海马神经元具有保护作用。
