Farombi Ebenezer O, Adedara Isaac A, Awoyemi Omolola V, Njoku Chinonye R, Micah Gabriel O, Esogwa Cynthia U, Owumi Solomon E, Olopade James O
Drug Metabolism and Toxicology Research Laboratories, Department of Biochemistry, College of Medicine, University of Ibadan, Ibadan, Nigeria.
Cancer Research and Molecular Biology Unit, Department of Biochemistry, College of Medicine, Nigeria.
Food Funct. 2016 Feb;7(2):913-21. doi: 10.1039/c5fo01228g.
The present study investigated the antioxidant and anti-inflammatory effects of dietary protocatechuic acid (PCA), a simple hydrophilic phenolic compound commonly found in many edible vegetables, on dextran sulphate sodium (DSS)-induced ulcerative colitis and its associated hepatotoxicity in rats. PCA was administered orally at 10 mg kg(-1) to dextran sulphate sodium exposed rats for five days. The result revealed that administration of PCA significantly (p < 0.05) prevented the incidence of diarrhea and bleeding, the decrease in the body weight gain, shortening of colon length and the increase in colon mass index in DSS-treated rats. Furthermore, PCA prevented the increase in the plasma levels of pro-inflammatory cytokines, markers of liver toxicity and markedly suppressed the DSS-mediated elevation in colonic nitric oxide concentration and myeloperoxidase activity in the treated rats. Administration of PCA significantly protected against colonic and hepatic oxidative damage by increasing the antioxidant status and concomitantly decreased hydrogen peroxide and lipid peroxidation levels in the DSS-treated rats. Moreover, histological examinations confirmed PCA chemoprotection against colon and liver damage. Immunohistochemical analysis showed that PCA significantly inhibited cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS) protein expression in the colon of DSS-treated rats. In conclusion, the effective chemoprotective role of PCA in colitis and the associated hepatotoxicity is related to its intrinsic anti-inflammatory and anti-oxidative properties.
本研究调查了膳食原儿茶酸(PCA)对葡聚糖硫酸钠(DSS)诱导的大鼠溃疡性结肠炎及其相关肝毒性的抗氧化和抗炎作用。PCA是一种常见于许多可食用蔬菜中的简单亲水性酚类化合物。以10 mg kg(-1)的剂量对暴露于葡聚糖硫酸钠的大鼠口服PCA,持续五天。结果显示,给予PCA可显著(p < 0.05)预防DSS处理的大鼠出现腹泻和出血、体重增加减少、结肠长度缩短以及结肠质量指数增加。此外,PCA可预防促炎细胞因子血浆水平升高、肝毒性标志物升高,并显著抑制DSS介导的处理大鼠结肠一氧化氮浓度升高和髓过氧化物酶活性。给予PCA通过提高抗氧化状态,显著保护结肠和肝脏免受氧化损伤,并同时降低DSS处理大鼠的过氧化氢和脂质过氧化水平。此外,组织学检查证实了PCA对结肠和肝脏损伤的化学保护作用。免疫组织化学分析表明,PCA可显著抑制DSS处理大鼠结肠中环氧合酶-2(COX-2)和诱导型一氧化氮合酶(iNOS)蛋白表达。总之,PCA在结肠炎及其相关肝毒性中的有效化学保护作用与其内在的抗炎和抗氧化特性有关。