黑曲霉抗高原病的药效学

来源 :中国医院药学杂志 | 被引量 : 0次 | 上传用户:bendehen123
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目的:研究黑曲霉(Aspergillus niger,AN)对常压下急性缺氧小鼠模型的抗缺氧作用。方法:将60只昆明小鼠随机分为Sham、Control、AN5、AN10、AN20和AN40组,每组10只。给予黑曲霉干预3 d后,采用常压密闭法建立缺氧模型,观察小鼠的存活时间,待小鼠死亡后,测定血(血清)、心、脑组织中血红蛋白(Hb)、脂质过氧化物(LPO)、总超氧化物歧化酶(T-SOD)、乳酸脱氢酶(LDH)的变化。结果:黑曲霉预处理明显延长小鼠常压下密闭缺氧的存活时间,与Sham组相比有统计学意义,分别为P<0.05或P<0.01;黑曲霉显著提升Hb含量,与Sham组相比有统计学意义,分别为P<0.05或P<0.01;黑曲霉剂量依赖性地减少心肌和脑组织的MDA生成,与Sham组比较差异具有统计学意义,P<0.05或P<0.01;黑曲霉增加血T-SOD活性,与Control组比较有统计学差异,P<0.05或P<0.01;黑曲霉可恢复缺氧所致的LDH活性,与Sham组比较具有统计学意义,P<0.05。结论:黑曲霉可延长缺氧状态下小鼠的存活时间,其作用是通过提升血清Hb含量、抑制脂质过氧化、增加T-SOD活性及恢复LDH活性实现的。 Objective: To study the anti-hypoxic effect of Aspergillus niger (AN) on acute hypoxic mouse model under normal pressure. Methods: Sixty Kunming mice were randomly divided into Sham, Control, AN5, AN10, AN20 and AN40 groups. After 3 days of intervention with Aspergillus niger, hypoxia model was established by normal pressure airtight method to observe the survival time of mice. After the death of mice, hemoglobin (Hb) and lipid in blood (serum), heart and brain were measured Oxide (LPO), total superoxide dismutase (T-SOD), lactate dehydrogenase (LDH) changes. Results: Aspergillus niger pretreatment significantly prolonged the survival time of hypoxia in mice under normal pressure, compared with Sham group, P <0.05 or P <0.01 respectively. Aspergillus niger significantly increased the content of Hb in Sham group P <0.05 or P <0.01 respectively; Aspergillus niger dose-dependently reduced the MDA production in myocardium and brain tissue, with statistical significance compared with Sham group (P <0.05 or P <0.01) Aspergillus niger increased blood T-SOD activity, compared with the Control group, there was a significant difference, P <0.05 or P <0.01; Aspergillus niger can restore LDH activity caused by hypoxia, compared with Sham group was statistically significant, P <0.05 . CONCLUSION: Aspergillus niger prolongs the survival time of mice under hypoxic condition by increasing serum Hb, inhibiting lipid peroxidation, increasing T-SOD activity and restoring LDH activity.
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