蝎毒缓激肽增强因子(BPF)对雄性白化大鼠四氯化碳(CCl4)肝损伤的抗氧化作用

Muhammad Salman
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引用次数: 4

摘要

本研究旨在探讨蝎毒缓激肽增强因子(BPF)对CCl4注射所致雄性白化大鼠肝损伤的治疗作用。体重250±20 g的雄性白化大鼠分为4组。在对照组;白化病大鼠腹腔注射100 L生理盐水。第二组(i.p)在100 L生理盐水溶液中注射BPF (1 gm/g)。每5天洗一次澡)。第3、4组小鼠每周2次腹腔注射0.5 ml/kg体重的CCl4,连续15 d,第4组小鼠仅在100 μL生理盐水溶液(1 μgm/g)中注射BPF。每5天洗一次澡)。结果表明,注射CCl4后30 d内血清过氧化氢酶(CAT)、超氧化物歧化酶(SOD)、还原性谷胱甘肽(GSH)、总蛋白和白蛋白均显著低于正常对照组。与正常对照动物相比,CCl4诱导丙二醛(MDA)、天冬氨酸氨基转移酶(AST)、丙氨酸氨基转移酶(ALT)和碱性磷酸酶(ALP)显著升高。BPF处理的效率是减轻CCl4对这些参数的影响。这些参数的改善可能归因于释放抗氧化剂和细胞因子和/或改善CCl4对肝脏的毒性作用。
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Antioxidant Effects of Bradykinin Potentiating Factor (BPF) Isolated from Scorpion Venom in Liver Injury Induced by Carbon Tetrachloride (CCl4) in Male Albino Rats
The main purpose of this study is to evaluate the ability of bradykinin potentiating factor (BPF) isolated from scorpion venom (Leiurus quinquestriatus) in treatment of liver injuries which induced by injection of CCl4 in male Albino rats. Male Albino rats (250±20 g body weight) were divided into four groups. In the control group; Albino rats were intraperitoneally (i.p) injected with 100 L saline solution. The second group (i.p) injected with BPF in 100 L saline solutions (1 gm/g. b. w. per 5 days). Third and fourth groups were i.p. injected with 0.5 ml/kg body weight (b. w.) twice weekly of CCl4 for fifteen days, after that only the fourth group was treated by BPF in 100 μL saline solutions (1 μgm/g. b. w. per 5 days). The results indicated that, CCl4 injection induced a significant decrease in serum catalase (CAT), Superoxide Dismutase (SOD), reduced glutathione (GSH), total protein and albumin, within thirty days post-injection of CCl4 as compared to the normal control group. In contrast, CCl4 induced a significant increase in Malondialdehyde (MDA), Aspartate Amino Transferase (AST), Alanine Amino Transferase (ALT), and Alkaline Phosphatase (ALP) compared to normal control animals. The efficiency of BPF treatment is alleviation the effects of CCl4 on these parameters. The improvement of these parameters may be attributed to the release antioxidant and cytokines and/or amelioration of the toxic effects of CCl4 on the liver.
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