Allicin Alleviates Inflammation of Trinitrobenzenesulfonic Acid-Induced Rats and Suppresses P38 and JNK Pathways in Caco-2 Cells

被引:51
作者
Li, Chen [1 ]
Lun, Weijian [1 ]
Zhao, Xinmei [1 ]
Lei, Shan [1 ]
Guo, Yandong [1 ]
Ma, Jiayi [1 ]
Zhi, Fachao [1 ]
机构
[1] Southern Med Univ, Nanfang Hosp, Dept Gastroenterol, Guangdong Prov Key Lab Gastroenterol, Guangzhou 510515, Guangdong, Peoples R China
基金
中国国家自然科学基金;
关键词
NF-KAPPA-B; HAPTEN-INDUCED MODEL; BOWEL-DISEASE; COLORECTAL-CANCER; DIALLYL DISULFIDE; KINASE PATHWAYS; GASTRIC-CANCER; COLON; ACTIVATION; EXPRESSION;
D O I
10.1155/2015/434692
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Background. Allicin has anti-inflammatory, antioxidative and proapoptotic properties. Aims. To evaluate the effects and investigate the mechanism of allicin on trinitrobenzenesulfonic acid-induced colitis, specifically with mesalazine or sulfasalazine. Methods. 80 rats were divided equally into 8 groups: control; trinitrobenzenesulfonic acid; allicin prevention; allicin; mesalazine; sulfasalazine; allicin + sulfasalazine, and mesalazine + allicin. Systemic and colonic inflammation parameters were analysed. In addition, protein and culture medium of Caco-2 cells treated with various concentrations of IL-1 beta or allicin were collected for investigation of IL-8, NF-kappa B p65 P38, ERK, and JNK. One-way ANOVA and Kruskal-Wallis H test were used for parametric and nonparametric tests, respectively. Results. Allicin reduced the body weight loss of trinitrobenzenesulfonic acid-induced rats, histological score, serum TNF-alpha and IL-1 beta levels, and colon IL-1 beta mRNA level and induced serum IL-4 level, particularly in combination with mesalazine. In addition, 1 ng/mL IL-1 beta stimulated the P38, ERK, and JNK pathways, whereas pretreatmentwith allicin depressed this phenomenon, except for the ERK pathway. Conclusions. The inflammation induced by trinitrobenzenesulfonic acid is mitigated significantly by allicin treatment, particularly combined with mesalazine. Allicin inhibits the P38 and JNK pathways and the expression of NF-kappa B which explained the potential anti-inflammatory mechanisms of allicin.
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页数:11
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