In this study, we investigated serum interleukin-1 beta (IL-1β) and tumor necrosis factor alpha (TNF-α) after ingestion of aflatoxin B1 (AFB1) in rats. We also studied the effects of nitric oxide (NO) on the stomach after consumption of AFB1. Therefore, we hypothesized that a standard anti-inflammatory agent-melatonin (MEL), and the flavonoid-rich fractions from Chromolaena odorata (FRFC) could counteract the deleterious effects of IL-1β, TNF-α, and NO after consumption of AFB1. Thirty-five Wistar rats (211.86 ± 27.23 g) were randomly selected into 5 groups, with 7 rats in each group. Group A (control); all rats in groups B, C, D, and E received 2.5 mg/kg AFB1 each orally on day 5, whereas those of groups C, D, and E received oral administration of 10 mg/kg MEL, 50 mg/kg FRFC1, and 100 mg/kg FRFC2, respectively, for 7 days. All of them were killed on the 8th day, 24 h after last treatment. Serum samples were analyzed for IL-1β and TNF-α, whereas stomach tissue was evaluated for NO level. Significant (P < 0.5) increase in serum IL-1β and TNF-α in rats given AFB1 only was recorded when compared with those in the control group. Conversely, we observed significant reduction in serum IL-1β and TNF-α in all the groups that received MEL, FRFC1, and FRFC2 after pretreatment with AFB1 when compared with those that were given AFB1 only. In addition, there was a significant increase in NO in rats given AFB1 only when compared with control, whereas reduction in NO was significant in the groups C, D, and E that were given MEL, FRFC1, and FRFC2, respectively, when compared with AFB1 group. MEL and FRFC may be responsible for the prevention of increased gastric mucosal NO and inflammatory effects of proinflammatory cytokines induced by AFB1.

中文翻译：

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Chromolaena odorata 褪黑激素和富含类黄酮的组分对 Wistar 大鼠胃粘膜中黄曲霉毒素 B1 诱导的促炎细胞因子和一氧化氮改变的影响。

在这项研究中，我们调查了大鼠摄入黄曲霉毒素 B1 (AFB1) 后的血清白细胞介素 1 β (IL-1β) 和肿瘤坏死因子 α (TNF-α)。我们还研究了消耗 AFB1 后一氧化氮 (NO) 对胃的影响。因此，我们假设标准抗炎剂褪黑激素 (MEL) 和来自 Chromolaena odorata (FRFC) 的富含类黄酮的部分可以抵消消耗 AFB1 后 IL-1β、TNF-α 和 NO 的有害影响。35只Wistar大鼠（211.86±27.23 g）随机分为5组，每组7只。A组（对照）；B、C、D 和 E 组的所有大鼠在第 5 天分别口服 2.5 mg/kg AFB1，而 C、D 和 E 组的所有大鼠口服给药 10 mg/kg MEL、50 mg/kg FRFC1，和 100 mg/kg FRFC2，分别为 7 天。全部在第8天，即最后一次治疗后24小时处死。分析血清样品的 IL-1β 和 TNF-α，而评估胃组织的 NO 水平。与对照组相比，仅给予 AFB1 的大鼠血清 IL-1β 和 TNF-α 显着增加（P < 0.5）。相反，我们观察到，与仅接受 AFB1 的组相比，接受 AFB1 预处理后接受 MEL、FRFC1 和 FRFC2 的所有组的血清 IL-1β 和 TNF-α 显着降低。此外，与对照组相比，仅给予 AFB1 的大鼠的 NO 显着增加，而与对照组相比，分别给予 MEL、FRFC1 和 FRFC2 的 C、D 和 E 组的 NO 减少显着AFB1 组。