Marmara University, School of Pharmacy, Department of Pharmacology, Tibbiye Cad. Haydarpaşa, Istanbul 34668, Turkey.
Environ Toxicol Pharmacol. 2007 Jan;23(1):25-32. doi: 10.1016/j.etap.2006.06.003. Epub 2006 Jun 15.
In this study, we investigated the protective effect of β-glucan against nicotine induced oxidative damage in urinary bladder and kidney tissues. Wistar albino rats were injected i.p. with nicotine hydrogen bitartarate (0.6mg/kg daily for 21 days) or saline. β-Glucan (50mg/kg, p.o.) was administered alone or with nicotine injections for 21 days. After decapitation, the urinary bladder and kidney tissues were taken for the measurement of malondialdehyde (MDA) and glutathione (GSH) levels, and myeloperoxidase (MPO) activity. Tissue samples were also examined histologically. In serum samples MDA, GSH, BUN, creatinine, TNF-α levels and LDH activity were analyzed. Chronic nicotine administration caused a significant decrease in GSH levels and increases in MDA levels and MPO activity in kidney and bladder tissues, suggesting oxidative organ damage, which was also histologically verified. Furthermore, β-glucan restored the reduced GSH levels, while it significantly decreased MDA levels and MPO activity. Renal function tests, LDH and TNF-α levels, which were increased significantly due to nicotine administration, were decreased with β-glucan treatment. The present data suggest that β-glucan supplementation effectively counteracts the chronic nicotine toxicity and attenuates oxidative damage of bladder and kidney tissues possibly by its antioxidant effects.
在这项研究中，我们研究了β-葡聚糖对尼古丁诱导的膀胱和肾脏组织氧化损伤的保护作用。Wistar 白化大鼠腹腔注射尼古丁酒石酸氢盐（每天 0.6mg/kg，连续 21 天）或生理盐水。β-葡聚糖（50mg/kg，po）单独或与尼古丁注射一起给药 21 天。断头后，取膀胱和肾脏组织测量丙二醛（MDA）和谷胱甘肽（GSH）水平以及髓过氧化物酶（MPO）活性。还检查了组织样本的组织学变化。在血清样本中分析 MDA、GSH、BUN、肌酐、TNF-α 水平和 LDH 活性。慢性尼古丁给药导致肾脏和膀胱组织中 GSH 水平降低，MDA 水平和 MPO 活性增加，提示发生氧化器官损伤，这也在组织学上得到了证实。此外，β-葡聚糖恢复了降低的 GSH 水平，同时显著降低了 MDA 水平和 MPO 活性。由于尼古丁给药而显著增加的肾功能测试、LDH 和 TNF-α 水平在 β-葡聚糖治疗后降低。这些数据表明，β-葡聚糖补充剂通过其抗氧化作用有效对抗慢性尼古丁毒性并减轻膀胱和肾脏组织的氧化损伤。
