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目的探讨蒿鳖养阴软坚方对牛血清白蛋白(BSA)免疫性肝纤维化大鼠的治疗作用。方法以18 mg/mL BSA与等体积的弗氏不完全佐剂混悬液足跖皮下多点注射5次免疫大鼠后,尾静脉攻击注射BSA生理盐水(每次2 mg/0.4 mL递增至3.4 mg/0.4 mL)15次,每周2次,制备肝纤维化模型;按体质量随机区组法分为模型组,蒿鳖养阴软坚方高、中、低剂量(8.2、2.59、0.82 g/kg,2.59 g/kg为临床等效剂量)组,复方鳖甲软肝片组,秋水仙碱组,各治疗组均于造模结束后ig给药(1 mL/100 g),每日1次,连续2个月,对照组和模型组分别ig等体积蒸馏水。酶谱法检测肝组织基质金属蛋白酶-2和-9(MMP-2、MMP-9),荧光法测定血清丙二醛(MDA),放免法检测血清透明质酸(HA)、层黏连蛋白(LN)、Ⅳ型胶原(Ⅳ-C)、Ⅲ型前胶原(PCⅢ)。结果蒿鳖养阴软坚方各剂量均能显著降低肝组织羟脯氨酸(Hyp)、MMP-2及MMP-9、肝纤维化程度、血清HA、LN、Ⅳ-C水平(P<0.05),其高、中剂量能明显降低血清MDA水平(P<0.05)。结论蒿鳖养阴软坚方对BSA免疫性肝纤维化大鼠具有治疗作用,抗脂质过氧化与降低MMP-2及MMP-9为其部分作用机制。
Objective To investigate the therapeutic effect of Artemisia turtle Yangyin Ruanjian Recipe on bovine serum albumin (BSA) autoimmune liver fibrosis in rats. Methods The rats were injected subcutaneously with 18 mg / mL BSA and an equal volume of Freund’s incomplete adjuvant suspension for 5 times. After BSA injection (2 mg / 0.4 mL each time) 3.4 mg / 0.4 mL) for 15 times twice a week for liver fibrosis model; according to the body mass randomized block method was divided into model group, Artemisia turtle Yangyin soft Jiangan high, medium and low doses (8.2,2.59,0.82 g / kg, 2.59 g / kg as clinical equivalent dose), Fufang Biejia Ruangan Tablet group, colchicine group and each treatment group were given ig administration (1 mL / 100 g) Day 1, for 2 consecutive months, the control group and the model group were equal volume of distilled water ig. The levels of MMP-2 and -9 (MMP-9, MMP-9) were detected by enzyme-linked immunosorbent assay (ELISA) and the levels of malondialdehyde (MDA) were measured by fluorescence spectrophotometry. Serum hyaluronic acid (HA), laminin (LN), type Ⅳ collagen (Ⅳ-C), type Ⅲ procollagen (PC Ⅲ). Results Each dose of Artemisia annua Softgels could significantly reduce the levels of Hyp, MMP-2 and MMP-9, the degree of hepatic fibrosis, the levels of serum HA, LN and Ⅳ-C in the liver tissues (P <0.05) , High and medium dose can significantly reduce serum MDA levels (P <0.05). Conclusion Artemisia turtle Yangyin Ruanjian has a therapeutic effect on BSA-induced auto-induced hepatic fibrosis in rats, and its anti-lipid peroxidation and its mechanism of decreasing MMP-2 and MMP-9 are part of the mechanism.