枸杞色素抑制脂多糖致大鼠葡萄膜炎作用与机制的研究

目的:探讨枸杞色素(lycium pigment)抑制脂多糖(LPS)致大鼠葡萄膜炎的作用及其机制.方法:枸杞色素(50,100,200 mg·kg-1)灌胃给药30 d后,足跖注射LPS建立大鼠葡萄膜炎模型.眼组织进行病理学检测；房水蛋白、一氧化氮和非对称性二甲基精氨酸(ADMA),眼组织诱导型一氧化氮合酶(iNOS)以及血清总抗氧化能力(T-AOC)、超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-PX)和脂质过氧化物丙二醛(MDA)分别采用Western blot、酶联免疫(ELISA)和生物化学等方法进行测定.结果:病理学研究显示,枸杞色素(50,100,200 mg·kg-1)显著降低LPS诱导的葡萄膜炎大鼠睫状体基质附近炎性细胞浸润渗出；降低眼内房水蛋白和一氧化氮生成的增多,并提高ADMA产生的减少.枸杞色素(100,200 mg·kg-1)显著抑制LPS诱导葡萄膜炎大鼠眼组织iNOS表达的增加.此外,枸杞色素(100,200 mg·kg-1)还可提高LPS诱导的葡萄膜炎大鼠血清T-AOC,SOD和GSH-PX活力的降低,并相应降低脂质过氧化物MDA的含量.结论:枸杞色素对LPS所致大鼠葡萄膜炎具有抑制作用,其机制与调控眼部一氧化氮/ADMA的水平和提高机体抗氧化能力有关.

Study on inhibitory effect of lycium pigment on lipopolysaccharide-induced uveitis in rats and its mechanism

Objective: To investigate the inhibitory effect of lycium pigment on lipopolysaccharide (LPS)-induced uveitis in rats and its mechanism. Method: The rat uveitis model was established by 30-day oral administration of lycium pigment (50, 100, 200 mg·kg^-1) and footpad injection of LPS. Ocular tissues were collected for a histopathological inspection. The protein, nitric oxide and ADMA in aqueous humor, level of inducible nitric oxide synthase (iNOS) in retina, activities of serum total antioxidant capacity (T-AOC), superoxide dismutase (SOD) and glutathione peroxidase (GSH-PX), and content of malondialdehyde (MDA) were determined by using Western blot, ELISA and biochemical methods. Result: According to the pathological study, lycium pigment (50, 100, 200 mg·kg^-1) could notably reduce the inflammatory cell infiltration around corpus ciliare matrix of uveitis rats, and the concentration of protein and nitric oxide, and increased ADMA in aqueous humor. Lycium pigment (100, 200 mg·kg^-1) could significantly inhibit the expression of iNOS in ocular tissues. In addition, lycium pigment (100, 200 mg·kg^-1) also decrease the activities of serum T-AOC, SOD, GSH-PX, and the content of lipid peroxide MDA. Conclusion: Lycium pigment has the inhibitory effect on LPS-induced uveitis in rats. Its mechanism is related to the regulation of nitric oxide/ADMA pathway and the improvement of oxidation resistance.