异贝壳杉烯酮可保护 PC12 细胞免受 H₂O₂诱导的氧化应激，并在 D-半乳糖衰老小鼠模型中发挥强大的抗衰老作用。
Isochaihulactone protects PC12 cell against H(2)O(2) induced oxidative stress and exerts the potent anti-aging effects in D-galactose aging mouse model.
机构信息
Department of Clinical Laboratory Science and Medical Biotechnology, College of Medicine National Taiwan University, Taipei, Taiwan, China.
出版信息
Acta Pharmacol Sin. 2010 Dec;31(12):1532-40. doi: 10.1038/aps.2010.152. Epub 2010 Nov 1.
AIM
to investigate the effect of isochaihulactone (also known as K8), a lignan compound of Bupleurum scorzonerifolium, on H(2)O(2)-induced cytotoxicity in neuronally differentiated PC12 cells (nPC12).
METHODS
viability of neuronal PC12 cells was measured using MTT assay. Protein expression was determined by Western blot. Apoptotic cells was determined using TUNEL assay. D-galactose aging mice were used as a model system to study the anti-oxidant effects of isochaihulactone in vivo.
RESULTS
pretreatment with isochaihulactone (5-10 micromol/L) increased cell viability and decreased membrane damage, generation of reactive oxygen species and degradation of poly (ADP-ribose) polymerase in H(2)O(2)-treated nPC12 cells and also decreased the expression of cyclooxygenase-2, via downregulation of NF-kappaB, resulting in a decrease in lipid peroxidation. The results suggest that isochaihulactone is a potential antioxidant agent. In a murine aging model, in which chronic systemic exposure to D-galactose (D-gal) causes the acceleration of senescence, administration of isochaihulactone (10 mgxkg(-1)xd(-1), sc) for 7 weeks concomitant with D-gal injection significantly increased superoxide dismutase and glutathione peroxidase activities and decreased the MDA level in plasma. Furthermore, H&E staining to quantify cell death within hippocampus showed that percentage of pyknotic nuclei in the D-gal-treated mice were much higher than in control.
CONCLUSION
the results suggest that isochaihulactone exerts potent anti-aging effects against D-gal in mice possibly via antioxidative mechanisms.
目的
研究柴胡素（亦称 K8）对神经分化 PC12 细胞（nPC12）中 H2O2 诱导细胞毒性的影响。
方法
用 MTT 分析法测定神经元 PC12 细胞的活力。用 Western blot 法测定蛋白表达。用 TUNEL 法测定凋亡细胞。用 D-半乳糖衰老小鼠模型系统研究体内柴胡素的抗氧化作用。
结果
用 5-10μmol/L 的柴胡素预处理可增加 H2O2 处理后的 nPC12 细胞的活力，减少膜损伤、活性氧生成和聚（ADP-核糖）聚合酶降解，同时降低环氧化酶-2 的表达，通过下调 NF-κB，减少脂质过氧化。结果表明柴胡素是一种有潜力的抗氧化剂。在 D-半乳糖（D-gal）慢性全身暴露导致衰老加速的小鼠衰老模型中，用柴胡素（10mgxkg(-1)xd(-1)，sc）连续 7 周处理，同时 D-gal 注射，可显著增加超氧化物歧化酶和谷胱甘肽过氧化物酶的活性，降低血浆 MDA 水平。此外，对海马内细胞死亡进行 H&E 染色定量显示，D-gal 处理组的固缩核百分比明显高于对照组。
结论
结果表明柴胡素通过抗氧化机制对 D-gal 诱导的小鼠具有明显的抗衰老作用。
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