Changes in serum cytokine levels, hepatic and intestinal morphology in aflatoxin B1-induced injury: modulatory roles of melatonin and flavonoid-rich fractions from Chromolena odorata

Changes in serum cytokine levels, hepatic and intestinal morphology in aflatoxin B1-induced injury: modulatory roles of melatonin and flavonoid-rich fractions from Chromolena odorata
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DOI:
10.1007/s12550-016-0239-9
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发表时间:
2016-05-01
期刊:
影响因子:
3
通讯作者:
Amid, Adetayo
Amid, Adetayo
中科院分区:
医学4区
文献类型:
--
作者:
Akinrinmade, Fadeyemi Joseph;Akinrinde, Akinleye Stephen;Amid, Adetayo

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已知黄曲霉毒素会产生慢性致癌、致突变和致畸作用,以及急性炎症作用,特别是在胃肠道中。本研究评估了富含黄酮的 Chromolena odorata (FCO) 提取物和褪黑激素(一种标准抗氧化剂和抗炎剂)对抗黄曲霉毒素 B1 (AFB1) 诱导的促炎细胞因子水平以及肝脏和小肠形态变化的潜力。我们使用Wistar白化大鼠(200-230g),随机分为五组,A组为对照大鼠; B组,大鼠在第5天和第7天给予AFB1(2.5 mg/kg,腹腔注射)两次; C、D和E组大鼠分别接受褪黑激素(10 mg/kg,腹腔注射)或口服FCO1(50 mg/kg)和FCO2(100 mg/kg)治疗7天,并在第5天和第7天注射AFB1。血清白细胞介素1β(IL-1β)和肿瘤坏死因子α水平 (TNF-α) 使用商业 ELISA 试剂盒进行测定,并对肝脏、十二指肠和回肠进行组织病理学评估。我们观察到血清 IL-1 β 显着升高(p < 0.05),与肝脏和肠道出血以及白细胞和淋巴细胞浸润相关,作为 AFB1 给药后急性炎症反应的证据。所有治疗均使 IL-1 β 水平显着降低 (p < 0.05),但无论进行何种治疗,接受 AFB1 的所有大鼠中 TNF-α 水平均未显着改变。褪黑激素和 FCO2 对肝组织产生了相当大的保护,尽管褪黑激素在保护肠道病变方面并不十分有效。我们的研究结果表明,细胞因子表达的调节可能在一定程度上导致了香花或褪黑激素改善与黄曲霉毒素 B1 损伤相关的肝脏和肠道损伤的能力。
Aflatoxins are known to produce chronic carcinogenic, mutagenic, and teratogenic effects, as well as acute inflammatory effects, especially in the gastrointestinal tract. The potentials of the flavonoid-rich extract from Chromolena odorata (FCO) and melatonin (a standard anti-oxidant and anti-inflammatory agent) against aflatoxin B1 (AFB1)-induced alterations in pro-inflammatory cytokine levels and morphology of liver and small intestines were evaluated in this study. We utilized Wistar albino rats (200-230 g) randomly divided into five groups made up of group A, control rats; group B, rats given AFB1 (2.5 mg/kg, intraperitoneal) twice on days 5 and 7; rats in groups C, D, and E were treated with melatonin (10 mg/kg, intraperitoneal) or oral doses of FCO1 (50 mg/kg) and FCO2 (100 mg/kg) for 7 days, respectively, along with AFB1 injection on days 5 and 7. Serum levels of interleukin 1 beta (IL-1 beta) and tumor necrosis factor alpha (TNF-alpha) were determined using commercial ELISA kits and histopathological evaluation of the liver, duodenum, and ileum were also carried out. We observed significant elevation (p < 0.05) in serum IL-1 beta correlating with hemorrhages and leucocytic and lymphocytic infiltration in the liver and intestines as evidences of an acute inflammatory response to AFB1 administration. All treatments yielded significant reduction (p < 0.05) in IL-1 beta levels, although TNF-alpha levels were not significantly altered in all rats that received AFB1, irrespective of the treatments. Melatonin and FCO2 produced considerable protection of hepatic tissues, although melatonin was not quite effective in protecting the intestinal lesions. Our findings suggest a modulation of cytokine expression that may, in part, be responsible for the abilities of C. odorata or melatonin in amelioration of hepatic and intestinal lesions associated with aflatoxin B1 injury.