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Curcumin exerts hepatoprotective effects via poorly defined mechanisms. Recently, some studies suggested that this effect was mediated by antagonizing CB1 receptors in hepatic stellate cells. The current study aimed to investigate whether CB1 antagonist, hemopressin, could potentiate the hepatoprotective effect of curcumin, in comparison with silymarin in bile duct-ligated (BDL) rats. Curcumin and hemopressin each alone and in combination ameliorated biochemical and structural fibrotic injury, and downregulated cyclooxygenase-2 (COX-2) and both mRNA and protein levels of nuclear factor kappa B (NF-κB) in fibrotic liver. In contrast to the previous studies, curcumin alone did not affect the gene expression of cannabinoid receptors. However, the combination of hemopressin and curcumin reduced the expression of CB1 in fibrotic liver. Surprisingly, silymarin upregulated CB2 receptors and downregulated CB1 at mRNA level more than all the administered drugs. Both curcumin and hemopressin each alone decreased lipid peroxidation product, malondialdehyde (MDA), while the combination increased the reduced glutathione content. All the administered drugs increased the hepatic antiapoptotic marker, Bcl2. Our study suggests that hemopressin potentiates the hepatoprotective effect of curcumin on fibrotic liver. We identified a new mechanism of the hepatoprotective effect of silymarin via modulation of cannabinoid receptors in fibrotic liver.

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Combretum micranthum is used traditionally for many therapeutic purposes such as fatigue, liver ailments, headache, convalescence, blood disease, weight loss among others. Studies suggested that free radical production may be one main reason behind stress induces neurochemical changes that include neurotransmitter imbalance and histopathological alterations in the brain cell. Thus this study examined the relationship between brain histopathological alterations and neurotransmitter imbalance (gamma aminobutyric acid - GABA) in lead exposure, and possible neuroprotective role of Combretum micranthum  methanol leaf extract in mice. Thirty six (36) Swiss Albino mice (19 - 22g body weight) were used for the study, randomized equally into six groups and treated for the period 14days:  a) Normal Control (Distilled water), b) Negative control (40 mg/kg lead acetate), c) lead acetate + 100 mg/kg b.w. extract, d) lead acetate + 50 mg/kg b.w. extract,  e) lead acetate + 25 mg/kg b.w. extract and f) positive control (lead acetate + diazepam 0.5 mg/kg b.w). The study assayed for protective potential of Combretum micranthum on neuronal cell membrane through determination of the brain cells malondialdyhyde (MDA) levels, morphology and GABA levels. Result of the study showed a significantly increase level of GABA in the brain of mice administered doses of the extract with a decreased level of MDA, as compared to those mice treated with 40 mg/kg lead acetate alone, which showed decreased level in GABA (310.83pg/ml), but an increased level of MDA (30.03μmolTBARS/mg). Also the mice administered doses of the extract showed normal neurons while intensive neuronal necrosis was observed on those mice treated with 40mg/kg lead acetate alone. However, mice administered with the doses of the extract shows no any significant difference with those in the normal control and positive control treatment groups.  Also the Combretum micranthum  methanol leaf extract was found, using GC-MS, to contain propargylamine, a compound known to possess anti-apoptosis functions, and also those with GABAergic functions 3,4-dichlorophenylhydrazine, guanidine and aminooxyacetic acid. Findings of the present study has proven Combretum micranthum to be a potential plant in managing and preventing brain structural damage induced by lead administration. Keywords: Lead, Combretum micranthum, GABA, malondialdyhyde (MDA) and histopathology

Background: Acrylamide (ACR) is a naturally occurring, widely used compound. Ingestion of large amounts of ACR underlies several health concerns and teratogenicity. Ascorbic acid (vitamin C) is a strong reducing agent greatly used to clean free radicals. This study investigated the morphometric, histological, immunohistochemical and biochemical disturbances induced by acrylamide (10 mg/kg/day) via gavage in the intestine of rat mothers and their offsprings. As well as, the protective role of ascorbic acid (100 mg/kg/day) via gavage. Materials and Methods: Forty adult pregnant female rats were divided into four groups; control, ascorbic acid, acrylamide and acrylamide+ascorbic acid. 10 randomly chosen offsprings of each group after weaning were also used. Histomorphometric analysis of intestinal wall and biochemical analysis of intestinal enzymes, oxidant antioxidant markers and some genes expression were performed. Results: In both dams and offsprings, ACR resulted in mucosal hyperplasia with evident inflammatory infiltration in the villi. In addition, goblet cells and KI67 +ve cell numbers decreased in the dams however increased in offsprings. ACR decreased citrate synthase, glutathione and catalase levels in dams and increased β-glucuronidase and malonaldehyde levels in dams. In offsprings, level of alkaline phosphatase was reduced and β-glucuronidase was elevated. Glutathione peroxidase and glutathione reductase mRNA expression was increased significantly with ACR ingestion. Ascorbic acid supplementation conserved the control status in the majority of conditions. Conclusion: Acrylamide consumption during pregnancy and lactation is risky because of the induction of intestinal mucosal hyperplasia in rat offsprings. Ascorbic acid supplementation could reduce the harmful effects induced by ACR.