Department of Physical Therapy, Hungkuang University, Taichung, Taiwan.
Department of Physical Therapy, Asia University, Taichung, Taiwan.
Am J Chin Med. 2020;48(2):373-390. doi: 10.1142/S0192415X20500196. Epub 2020 Mar 5.
The medicinal plant grows at high altitudes in the Arctic and mountainous regions and is commonly used in phytotherapy in Eastern European and Asian countries. In the present study, we investigated the anti-apoptotic effect of and its neuroprotective mechanism of action in a rat model of D-galactose-induced aging. Two groups of twelve-week-old male Wistar rats received a daily injection of D-galactose (150mg/kg/day, i.p.) and orally administered (0, 248mg/kg/day) for eight weeks, while a control group received a saline injection (1ml/kg/day, i.p.). We examined apoptosis in the cortex and hippocampus of three groups of rats based on a terminal deoxynucleotide transferase-mediated deoxy uridine triphosphate nick-end labeling (TUNEL) positive assay. The expression levels of apoptotic and anti-apoptotic proteins in excised brains were analyzed by Western blotting. Our findings indicated that D-galactose caused marked neuronal apoptosis via activation of both extrinsic-dependent and mitochondrial-dependent apoptotic pathways. When compared to the control group, the protein levels of Fas receptor, Fas ligand, Fas-associated death domain (FADD), and activated caspase-8 (Fas-dependent apoptotic pathways), as well as those of t-Bid, Bax, cytochrome , activated caspase-9, and activated caspase-3 (mitochondrial-dependent apoptotic pathways), were significantly increased in the D-galactose treated group. In addition, D-galactose impaired the phosphorylation of PI3K/Akt, an important survival signaling event in neurons. , however, protected against all these neurotoxicities in aging brains. The present study suggests that neuronal survival promoted by may be a potentially effective method to enhance the resistance of neurons to age-related disorders.
药用植物生长在高寒地区的北极和山区，常用于东欧和亚洲国家的植物疗法。在本研究中，我们研究了 对 D-半乳糖诱导衰老大鼠的抗凋亡作用及其神经保护作用机制。两组 12 周龄雄性 Wistar 大鼠每天腹腔注射 D-半乳糖（150mg/kg/天）并口服 （0、248mg/kg/天）8 周，对照组注射生理盐水（1ml/kg/天，腹腔内）。我们根据末端脱氧核苷酸转移酶介导的脱氧尿苷三磷酸缺口末端标记（TUNEL）阳性测定法，检查三组大鼠皮质和海马中的细胞凋亡。通过 Western blot 分析切除脑组织中凋亡和抗凋亡蛋白的表达水平。我们的研究结果表明，D-半乳糖通过激活外源性和线粒体依赖性凋亡途径导致明显的神经元凋亡。与对照组相比，D-半乳糖处理组 Fas 受体、Fas 配体、Fas 相关死亡结构域（FADD）和激活的 caspase-8（Fas 依赖性凋亡途径）以及 t-Bid、Bax、细胞色素、激活的 caspase-9 和激活的 caspase-3（线粒体依赖性凋亡途径）的蛋白水平显着升高。此外，D-半乳糖损害了神经元中重要的生存信号事件 PI3K/Akt 的磷酸化。 ，然而，在衰老大脑中可以防止所有这些神经毒性。本研究表明， 通过 促进神经元存活可能是增强神经元对与年龄相关疾病的抵抗力的一种有效方法。
