Objective To observe the effects of Siweiyuganzi prescription on anti-peroxidation and blood lipid levels in experimental rats with hyperlipidemia. Methods Sixty male Sprague-Dawley (SD) rats were divided into normal control group, hyperlipidemia model group, Xuezhikang group, Siweiyuganzi prescription large, medium and small dose group according to the random number table method, with 10 rats in each group. The hyperlipidemia rat model was established by intragastric feeding with high fat emulsion everyday 10 mL·kg-1·d-1; normal saline 10 mL/kg was given to the normal control group, twice a day by intragastric feeding; 3 dosages of Siweiyuganzi suspended fluid 12.8, 6.4, 4.3 g·kg-1·d-1 intragastric administrations were given to Siweiyuganzi prescription large, medium and small dose groups respectively; Xuezhikang suspended fluid 0.3 g·kg-1·d-1 was given to Xuezhikang group intragastrically;the same volume of normal saline was given to hyperlipidemia model group. After 4 weeks, the level changes of blood lipid, serum superoxide dismutase (SOD), malonaldehyde (MDA), hydroxymethylglutaryl Coenzyme A (HMG-CoA) were observed. Results Compared to those in the normal control group, the levels of triglyceride (TG), total cholesterol (TC), low density lipoprotein cholesterol (LDL-C), MDA, content and positive expression of HMG-CoA, alanine aminotransferase (ALT) were all higher in hyperlipidemia model group [TG (mmol/L): 6.59±0.72 vs. 4.32±0.36, TC (mmol/L): 7.10±0.25 vs. 5.98±0.40, LDL-C (mmol/L): 4.18±1.30 vs. 2.33±0.35, MDA (μmol/L): 26.05± 5.99 vs. 10.08±1.98, HMG-CoA content (ng/L): 54.60±2.90 vs. 48.73±3.09, HMG-CoA positive expression in liver tissue:(57.80±12.30)% vs. (22.00±4.92)%, ALT (U/L): 106.83±15.75 vs. 81.97±13.18]; SOD and high-density lipoprotein cholesterol (HDL-C) in hyperlipidemia model group were significantly decreased [SOD (kU/L): 295.47±37.51 vs. 345.13±19.76, HDL-C (mmol/L): 2.32±0.49 vs. 4.84±0.45, both P < 0.05]. Compared with the hyperlipidemia model group, the TG, TC, LDL-C, MDA, contents and positive expression of HMG-CoA in each group were significantly reduced, and the SOD and HDL-C were obviously increased, and the changes in the Siweiyuganzi high dose group were more significant than those of the Siweiyuganzi middle-and low-dose groups [TG (mmol/L): 4.70±0.46 vs. 5.40±0.31, 5.70±0.41, TC (mmol/L): 5.80±0.23 vs. 6.14±0.20, 6.56±0.32, LDL-C (mmol/L): 2.56±0.45 vs. 2.93±0.33, 3.28±0.32, HDL-C (mmol/L): 4.58±0.28 vs. 3.89±0.30, 3.59±0.08, SOD (kU/L): 381.45±20.68 vs. 360.60±30.16, 325.49±32.13, MDA (μmol/L): 16.98±5.39 vs. 17.89±5.37, 21.03±6.01, HMG-CoA content (ng/L): 50.58±0.77 vs. 52.16±0.66, 52.90±0.91, HMG-CoA positive expression in liver tissue: (27.90±6.03)% vs. (32.20±7.00)%, (43.00±8.39)%, all P < 0.05]. In the normal control group, there were positive cells scattered in the central vein area and loosely distributed around the portal area in the rat liver; in the hyperlipidemia model group, the positive cells were increased in the central vein area and the cells in relatively great number were seen around the portal area. While the positive cells in Xuezhikang group and in the high, medium and low dose Siweiyuganzi groups were decreased. Conclusion Siweiyuganzi prescription can regulate the levels of blood lipids, prevent and treat the lipid peroxidation caused by hyperlipidemia, and inhibit excessive expression of HMG-CoA in experimental rats with hyperlipidemia.%目的 观察藏药复方四味余甘子方对实验性高脂血症模型大鼠抗过氧化和血脂水平的影响.方法 选择雄性SD大鼠60只,按随机数字表法分为正常对照组、高脂血症模型组、血脂康组、四味余甘子方大、中、小剂量组,每组10只.采用灌服10 mL·kg-1·d-1高脂乳剂的方法复制高脂血症动物模型.正常对照组和高脂血症模型组灌胃生理盐水10 mL/kg、每日2次;四味余甘子方组以12.8、6.4、4.3 g·kg-1·d-1 3个剂量灌胃;血脂康组灌胃0.3 g·kg-1·d-1血脂康混悬液.4周后,观察各组血脂和血清超氧化物歧化酶(SOD)、丙二醛(MDA)、羟甲基戊二酰辅酶A(HMG-CoA)还原酶水平的变化.结果 与正常对照组比较,高脂血症模型组血清三酰甘油(TG)、总胆固醇(TC)、低密度脂蛋白胆固醇(LDL-C)、MDA、HMG-CoA含量和肝组织HMG-CoA阳性表达、丙氨酸转氨酶(ALT)水平均明显升高〔TG(mmol/L):6.59±0.72比4.32±0.36,TC(mmol/L):7.10±0.25 比 5.98±0.40,LDL-C(mmol/L):4.18±1.30 比 2.33±0.35,MDA(μmol/L):26.05±5.99 比10.08±1.98,HMG-CoA含量(ng/L):54.60±2.90比48.73±3.09,HMG-CoA阳性表达:(57.80±12.30)%比(22.00±4.92)%,ALT(U/L):106.83±15.75比81.97±13.18〕,SOD、高密度脂蛋白胆固醇(HDL-C)明显降低〔SOD(kU/L):295.47±37.51比345.13±19.76,HDL-C (mmol/L):2.32±0.49比4.84±0.45,均P＜0.05〕.与高脂血症模型组比较,各给药组TG、TC、LDL-C、MDA和HMG-CoA含量以及肝组织阳性表达均明显降低,SOD、HDL-C均明显升高,且以四味余甘子方大剂量组的变化较四味余甘子方中、小剂量组更显著〔TG(mmol/L):4.70±0.46 比 5.40±0.31、5.70±0.41,TC(mmol/L):5.80±0.23 比 6.14±0.20、6.56±0.32,LDL-C(mmol/L):2.56±0.45 比 2.93±0.33、3.28±0.32,HDL-C(mmol/L):4.58±0.28 比 3.89±0.30、3.59±0.08,SOD(kU/L):381.45±20.68 比 360.60±30.16、325.49±32.13,MDA(μmol/L):16.98±5.39 比 17.89±5.37、21.03±6.01, HMG-CoA含量(ng/L):50.58±0.77比52.16±0.66、52.90±0.91,肝组织HMG-CoA阳性表达:(27.90±6.03)%比(32.20±7.00)%、(43.00±8.39)%,均P＜0.05〕.正常对照组大鼠肝脏中央静脉区可见散在分布的阳性细胞;汇管区可见疏松分布的阳性细胞,高脂血症模型组大鼠肝脏中央静脉区阳性细胞增多,汇管区周围见到较多的阳性细胞,四味余甘子方大、中、小剂量组及血脂康组阳性细胞减少.结论 四味余甘子方能调节血脂,防治高脂血症引起的脂质过氧化反应,抑制HMG-CoA的过度表达.
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