Berberine Recovered Oxidative Stress Induced by Sodium Nitrite in Rat Erythrocytes.

Morteza Akhzari, Mahdi Barazesh, Sajad Jalili, Mohammad Mahdi Farzinezhadi Zadeh
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引用次数: 2

Abstract

Objective: Berberine, a plant derived alkaloid, present in Berberis species is well known as one of the most important antioxidants. The current research aimed to study the heamatoprotective characteristics of berberine and clarify its plausible mechanisms against sodium nitrite.

Methods: Forty numbers of male Sprague Dawley rats were categorized into five equal groups, including group 1: control (normal saline); group 2: berberine (100 mg/kg); group 3: sodium nitrite (80 mg/kg); group 4: sodium nitrite (80 mg/kg) plus berberine (50 mg/kg) and group 5: sodium nitrite (80 mg/kg) plus berberine (100 mg/kg) groups. All animals were orally administrated for two months once daily. At the end of the 60th day, blood samples were withdrawn by cardiac puncture and collected in test vials when the animals had been anesthetized with ketamine (70 mg/kg). Then, hemolysate was prepared and the oxidative stress biomarkers, lipid peroxidation, and antioxidant capacity of erythrocytes were evaluated.

Results: Feeding of rats with sodium nitrite remarkably enhanced malondialdehyde (MDA) (p=0.001) levels and considerably reduced the levels of glutathione (GSH) (p=0.001), and also reduced the enzymatic activities of glutathione peroxidase (GPx) (p=0.02), superoxide dismutase (SOD) (p=0.001), glutathione reductase (GR) (p=0.02), and catalase (CAT) (p=0.01). However, the co-administration of these animals with 100 mg/kg of berberine remarkably reverted the values to reach nearly a normal level. While 50 mg/kg berberine failed to restore significantly all of these antioxidant biomarkers at a normal level.

Conclusion: Our results clearly demonstrated that berberine in a dose-dependent manner led to protection against sodium nitrite-induced oxidative injury in rat erythrocytes, which possibly reflects the antioxidant ability of this alkaloid.

小檗碱恢复亚硝酸钠所致大鼠红细胞氧化应激。
目的:小檗碱是一种植物源性生物碱,存在于小檗属植物中,是最重要的抗氧化剂之一。本研究旨在研究小檗碱的热保护特性,阐明其对亚硝酸钠的作用机制。方法:选取雄性sd大鼠40只,随机分为5组:1组:对照组(生理盐水);第二组:小檗碱(100 mg/kg);第三组:亚硝酸钠(80 mg/kg);第4组:亚硝酸钠(80 mg/kg) +小檗碱(50 mg/kg)组;第5组:亚硝酸钠(80 mg/kg) +小檗碱(100 mg/kg)组。所有动物口服给药2个月,每日1次。第60天结束时,在氯胺酮(70 mg/kg)麻醉的情况下,采用心脏穿刺取血,装入试验瓶。然后制备溶血液,评估红细胞氧化应激生物标志物、脂质过氧化和抗氧化能力。结果:亚硝酸钠喂养大鼠显著提高丙二醛(MDA)水平(p=0.001),显著降低谷胱甘肽(GSH)水平(p=0.001),降低谷胱甘肽过氧化物酶(GPx) (p=0.02)、超氧化物歧化酶(SOD) (p=0.001)、谷胱甘肽还原酶(GR) (p=0.02)和过氧化氢酶(CAT) (p=0.01)的酶活性。然而,给这些动物同时服用100毫克/公斤的小檗碱后,这些数值明显恢复到接近正常水平。而50mg /kg小檗碱不能显著恢复所有这些抗氧化生物标志物在正常水平。结论:小檗碱对亚硝酸钠诱导的大鼠红细胞氧化损伤具有剂量依赖性的保护作用,这可能反映了小檗碱的抗氧化能力。
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