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目的探讨黄连解毒汤(Huanglian Jiedu Decoction,HJD)对动脉粥样硬化大鼠血气指标的影响。方法雄性SD大鼠,随机分成正常对照组、模型组、洛伐他丁组及黄连解毒汤低、中、高3个剂量组,每组10只。除正常对照组喂普通饲料外,其余喂以高脂饲料,同时定期注射维生素D_3,造模8周,从第3周开始每天灌胃给药1次。造模结束后于腹主动脉取血,测定相关指标。结果血脂结果显示:与正常对照组比较,模型组的总胆固醇(TC)、甘油三酯(TG)、低密度脂胆固醇(LDL)显著上升,高密度脂胆固醇(HDL)显著下降(P<0.05);给药后,各组均可显著降低LDL、TG指标,阳性对照组和HJD低剂量组可显著降低TC指标,且高剂量组可显著升高HDL指标(P<0.05)。血气分析结果显示:与正常对照组比较,造模后,动脉氧分压(pO_2)极显著下降(P<0.001),二氧化碳分压(pCO_2)、二氧化碳总量(pCO_2(T))显著上升(P<0.05);给药后,除黄连解毒汤高剂量组,其余各组均可显著升高pO_2(P<0.05),但对pCO_2、pCO_2(T)无显著性影响(P>0.05)。各组pH值均无显著差异(P>0.05)。结论黄连解毒汤对动脉粥样硬化大鼠可起到一定干预作用,推测其作用机制为改善大鼠的氧分压。
Objective To investigate the effect of Huanglian Jiedu Decoction (HJD) on blood gas indexes in atherosclerotic rats. Methods Male Sprague-Dawley rats were randomly divided into normal control group, model group, lovastatin group and Huanglian Jiedu Decoction low, medium and high dose groups of 10, each group. In addition to the normal control group fed normal feed, the other fed with high-fat diet, while regular injection of vitamin D_3, modeling for 8 weeks, starting from the third week of gavage once a day. Abdominal aorta blood after modeling, the determination of relevant indicators. Results The results of blood lipids showed that TC, TG, LDL and HDL in model group were significantly lower than those in normal control group (P <0.05) After administration, LDL, TG, positive control group and HJD low dose group could significantly reduce TC index, and high-dose group could significantly increase HDL index (P <0.05). Results of blood gas analysis showed that after modeling, the arterial oxygen partial pressure (pO_2) significantly decreased (P <0.001) and the partial pressure of carbon dioxide (pCO_2) and total carbon dioxide (pCO_2 (T)) increased significantly P <0.05). After administration, except for Huanglianjiedu Decoction high dose group, the other groups could significantly increase pO_2 (P <0.05), but had no significant effect on pCO_2 and pCO_2 (T) (P> 0.05). There was no significant difference in pH between groups (P> 0.05). Conclusion Huanglian Jiedu Decoction may play an intervention role in atherosclerosis rats, suggesting that its mechanism of action is to improve the oxygen partial pressure in rats.