Allicin alleviates inflammation of trinitrobenzenesulfonic acid-induced rats and suppresses P38 and JNK pathways in Caco-2 cells.
Allicin alleviates inflammation of trinitrobenzenesulfonic acid-induced rats and suppresses P38 and JNK pathways in Caco-2 cells.
复制标题
大蒜素减轻三硝基苯磺酸诱导的大鼠炎症并抑制 Caco-2 细胞中的 P38 和 JNK 通路
DOI：
10.1155/2015/434692
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发表时间：
2015
影响因子：
4.6
通讯作者：
Zhi F
中科院分区：
文献类型：
--
作者：
Li C;Lun W;Zhao X;Lei S;Guo Y;Ma J;Zhi F
背景大蒜素具有抗炎、抗氧化和促细胞凋亡的特性。目标。评价大蒜素对三硝基苯磺酸诱导的结肠炎的作用，并探讨其作用机制。方法.将80只大鼠平均分为8组：对照组、三硝基苯磺酸组、大蒜素预防组、大蒜素组、美沙拉秦组、柳氮磺胺吡啶组、大蒜素+柳氮磺胺吡啶组和美沙拉秦+大蒜素组。分析全身和结肠炎症参数。另外，收集用不同浓度的IL-1β或大蒜素处理的Caco-2细胞的蛋白质和培养基，用于研究IL-8、NF-κB p65 P38、ERK和JNK。单因素方差分析和Kruskal-Wallis H检验分别用于参数和非参数检验。结果大蒜素可降低三硝基苯磺酸诱导的大鼠体重减轻、组织学评分、血清TNF-α和IL-1β水平、结肠IL-1β mRNA水平和诱导的血清IL-4水平，尤其是与美沙拉秦联合使用时。此外，1 ng/mL IL-1β刺激P38、ERK和JNK通路，而大蒜素预处理抑制了这种现象，但ERK通路除外。结论.大蒜素治疗，特别是与美沙拉秦联合治疗，可显著减轻三硝基苯磺酸诱导的炎症。大蒜素通过抑制P38和JNK通路及NF-κB B的表达，解释了大蒜素潜在的抗炎机制。
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-1β or allicin were collected for investigation of IL-8, NF-κB 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-α and IL-1β levels, and colon IL-1β mRNA level and induced serum IL-4 level, particularly in combination with mesalazine. In addition, 1 ng/mL IL-1β stimulated the P38, ERK, and JNK pathways, whereas pretreatment with 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-κB which explained the potential anti-inflammatory mechanisms of allicin.
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影响因子：
32.4
作者：
Garlanda C;Dinarello CA;Mantovani A
通讯作者：
Mantovani A
影响因子：
56.9
作者：
Johnson, GL;Lapadat, R
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Lapadat, R
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29.4
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4.2
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9.8
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Jess, Tine;Loftus, Edward V., Jr.;Sandborn, William J.
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