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-1β) and tumor necrosis factor alpha (TNF-α) 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-1β 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-1β levels, although TNF-α 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.

Parquetina nigrescens is a medicinal herb with recognized antioxidant properties and potential to alleviate conditions associated with oxidative stress, including gastric ulcers. We investigated the protective potential of methanol extract of Parquetina nigrescens (MEPN) against ischemia-reperfusion injury in the intestine of rats. Thirty (30) male Wistar albino rats were randomly assigned into five groups with Group I made up of control rats and Group II consisting of rats experimentally subjected to ischemia and reperfusion (IR) by clamping of the superior mesenteric artery (SMA) for 30 minutes and 45 minutes, respectively. Groups III and IV rats also had IR, but were initially pre-treated with MEPN at 500 mg/kg and 1000 mg/kg respectively, for seven days. Rats in Group V were also pre-treated with Vitamin C, for seven days, before induction of IR. The results showed marked reduction in intestinal epithelial lesions in groups treated with MEPN, compared to the IR group which had severe villi erosion, inflammatory cell infiltration and hemorrhages. There were significant increases in Malondialdehyde (MDA) and significant reductions in reduced glutathione (GSH) and Glutathione S-transferase (GST) activity with IR injury, while pre-treatment with either MEPN or Vitamin C prevented these effects. Increases in Glutathione peroxidase (GPX), Catalase (CAT) and Superoxide dismutase (SOD) with IR provided evidence for adaptive responses to oxidative injury during IR and preservation of enzyme activity by MEPN and Vitamin C. Taken together, Parquetina nigrescens provided considerable alleviation of intestinal injury produced by IR, at values much as effective as that offered by Vitamin C.

Background: Moringa oleifera is known to exhibit protection against oxidative damage due to its rich content of compounds with antioxidant activity. This study investigated the protective effect of the methanol extract of Moringa oleifera (MO) in a rat model of renal ischemia-reperfusion (IR) injury. Methods: Forty two wistar rats were randomly assigned to six groups of seven rats each, as follows: A, control group; B, sham-operated group; C, IR group; D, IR + low dose (200 mg/kg) MO; E, IR + high dose (400 mg/kg) MO and F, IR + Vitamin C (200 mg/kg). Unilateral ischaemia was induced by occluding the left renal artery for 45 minutes followed by rep- erfusion up to 24 hours. Results: Moringa oleifera significantly (p<0.05) ameliorated IR-induced increases in malondialdehyde (MDA), protein carbon- yls (PC) and advanced oxidation protein products (AOPP), while also decreasing serum BUN and Creatinine levels. More- over, the low dose of MO caused reductions in renal NO and H2O2 levels, while increasing renal GPx and GST activities. Histopathology revealed marked improvement of tissue alterations induced by IR with both doses of MO. Conclusion: Overall, the methanol extract of M. oleifera effectively attenuated the deleterious effects of renal IR via allevi- ation of tissue oxidative stress. Keywords: Oxidative stress; ischaemia-reperfusion; Moringa oleifera; kidneys; antioxidants.

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In this study, we investigated serum interleukin-1 beta (IL-1b) and tumor necrosis factor alpha (TNF-a) 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-1b, TNF-a, 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 FRFC 1 , and 100 mg/kg FRFC 2 , respectively, for 7 days. All of them were killed on the 8th day, 24 h after last treatment. Serum samples were analyzed for IL-1b and TNF-a, whereas stomach tissue was evaluated for NO level. Significant (P < 0.5) increase in serum IL-1b and TNF-a in rats given AFB1 only was recorded when compared with those in the control group. Conversely, we observed significant reduction in serum IL-1b and TNF-a in all the groups that received MEL, FRFC 1 , and FRFC 2 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, FRFC 1 , and FRFC 2 , 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.