姜黄素对酒精诱导的大鼠脂质过氧化反应的影响

Effect of curcumin on alcohol-induced lipid peroxidation in rats

目的:观察姜黄素对酒精性肝病大鼠肝脏氧化应激指标SOD,MDA和NO及血清ALT,AST和ALP水平的影响,探讨姜黄素对酒精诱导的大鼠脂质过氧化反应的影响.方法:将40只SD大鼠随机分为对照组、模型组、姜黄素治疗Ⅰ组(40 mg/kg)、姜黄素治疗Ⅱ组(80 mg/kg)和姜黄素治疗Ⅲ组(160mg/kg),每组8只.除对照组用等量生理盐水灌胃外,其他组均采用56度白酒6.72 g/(kg·d)灌胃的方法制作酒精性肝病大鼠模型,6 wk后姜黄素治疗Ⅰ、Ⅱ、Ⅲ组分别加用姜黄素ig,至12 wk末,处死大鼠,抽取血标本测定血清ALT、AST及ALP水平;留取肝组织标本测定SOD活性、MDA及NO含量,常规HE染色观察肝脏病理变化.结果:与对照组相比,模型组大鼠血清ALT、AST及ALP水平显著升高(86.4±7.5 vs 33.5±10.3;201.0±16.8 vs 116.5±12.0;205.1±20.0 vs 104.6±9.4;均P<0.01);肝组织SOD活性明显下降(80.21±4.55 vs 180.24±27.53,P<0.01),MDA及NO含量显著升高(3.29±0.34vs 1.35±0.12;4.37±0.21 vs 2.72±0.13;均P<0.01).与模型组相比,各姜黄素治疗组血清ALT、AST及ALP水平(Ⅰ组:66.5±9.6,171.4±10.8,176.4±13.7;Ⅱ组:52.4±12.0,145.8±11.9,146.9±13.8;Ⅲ组:40.9±7.9,135.0±11.8,127.1±12.6)明显降低(P<0.05或P<0.01),肝组织MDA及NO含量(Ⅰ组:2.84±0.27,4.01±0.17;Ⅱ组:1.95±0.23,3.60±0.16;Ⅲ组:1.65±0.08,3.22±0.13)均显著降低(P<0.05或P<0.01),而SOD活性(92.36±6.47,117.69±21.96,146.70±27.36)明显提高(P<0.05或P<0.01),其中以Ⅱ、Ⅲ治疗组较为显著.模型组大鼠肝细胞出现不同程度的脂肪变性,伴有点、灶状坏死,炎性细胞浸润,各姜黄素治疗组肝脏病理变化不同程度的轻于模型组.结论:姜黄素能抑制脂质过氧化,减轻或防治酒精诱导的肝损伤.

AIM： To reproduce an experimental rat model of alcoholic liver disease, and to investigate the effect of curcumin on lipid peroxidation induced by alcohol in rats. METHODS： Forty Sprague-Dawley rats were randomly divided into 5 groups （n = 8）： control group, model group, and three curcumin treatment （40, 80, 160 mg/kg） groups. Rats in the control group were intragastrically infused with normal saline, and those in the other groups were intragastrically infused with 560 mL/L alcohol （6.72 g/kg per day）. After 6 wk, curcumin was added to rats in the curcumin treatment groups at 40, 80, and 160 mg/kg, respectively. At the end of the 12th wk, all of the rats were killed. The levels of serum alanine aminotransferase （ALT）, aspartate aminotransferase （AST） and alkaline phosphatase （ALP） were measured. Liver samples were collected for determinationof superoxide dismutase （SOD）, malondialdehyde （MDA） and nitric oxide （NO） contents and routine histological examination. RESULTS： In comparison with those in the control group, the serum ALT, AST and ALP levels （86.4 ± 7.5 vs 33.5 ± 10.3; 201.0 ± 16.8 vs 116.5 ± 12.0; 205.1 ± 20.0 vs 104.6 ± 9.4; all P 〈 0.01） and the tissue contents of MDA and NO （3.29 ± 0.34 vs 1.35 ± 0.12; 4.37 ± 0.21 vs 2.72 ± 0.13; both P 〈 0.05） were significantly increased in the model group, but SOD activity was markedly decreased （80.21 ± 4.55 vs 180.24 ± 27.53, P 〈 0.01）. However, curcumin markedly down-regulated the levels of serum ALT, AST and ALP （40 mg/kg： 66.5 ± 9.6, 171.4 ± 10.8, 176.4 ± 13.7; 80 mg/kg： 52.4 ± 12.0, 145.8 ± 11.9, 146.9 ± 13.8; 160 mg/kg： 40.9 ± 7.9, 135.0 ± 11.8, 127.1 ± 12.6; P 〈 0.05 or P 〈 0.01）, as well as the tissue contents of MDA and NO （40 mg/kg： 2.84 ± 0.27, 4.01 ± 0.17; 80 mg/kg： 1.95 ± 0.23, 3.60 ± 0.16; 160 mg/kg： 1.65 ± 0.08, 3.22 ± 0.13; P 〈 0.05 or P 〈 0.01）. Inversely, the activity of SOD was elevated （92.36 ± 6.47, 117.69 ± 21.96, 146.70 ± 27.36; P 〈 0.05 or P 〈 0.01）. Histological examination showed fatty degeneration, focal necrosis and inflammatory cell infi ltration in the model group, but the changes were milder in the curcumin treatment groups at variable degrees. CONCLUSION： Curcumin can prevent alcohol-induced liver injury in rats by inhibiting lipid peroxidation.