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Item 6-Gingerol delays tumorigenesis in benzo[a]pyrene and dextran sulphate sodium-induced colorectal cancer in mice(Elsevier Ltd., 2020) Farombi, E. O. || ||; Ajayi, B. O.; Adedara, I. A.Colorectal cancer (CRC) has been linked to dietary consumption of benzo[a]pyrene (B[a]P). 6-Gingerol (6-G), a component of ginger has been reported to possess anti-inflammatory and antioxidant activities, but little is known regarding the mechanism of 6-G in CRC chemoprevention. We therefore investigated the effect of 6-G on B[a]P. and dextran sulphate sodium (DSS) induced CRC in mice. Mice in Group I and Group II received corn oil and 6-G orally at 2 ml/kg and 100 mg/kg, respectively for 126 days. Group III were administered 125 mg/kg of B [a]P for 5 days followed by 3 cycles of 4% dextran sulphate sodium (DSS). Group IV received 6-G for 7 days followed by co-administration with 125 mg/kg of B[a]P. for 5 days and 3 cycles of 4% DSS. Tumor formation was reduced and expression of Ki-67, WNT3a, DVL-2 and p-catenin following 6-G exposure. Also, 6-G increases expression of APC, P53, TUNEL positive nuclei and subsequently decreased the expression of TNF-a, IL-1p, INOS, COX-2 and cyclin D1. 6-G inhibited angiogenesis by decreasing the concentration of VEGF, Angiopoietin- 1, FGF and GDF-15 in the colon of B[a]P. and DSS exposed mice. Overall, 6-G attenuated B[a]P and DSS-induced CRC in mice via anti-inflammatory, anti-proliferative and apoptotic mechanisms.Item Protocatechuic acid modulates reproductive dysfunction linked to furan exposure in rats(Elsevier B.V., 2020) Owumi, S. E.; Adedara, I. A.; Farombi, E. O.; Oyelere, A. K.The reproductive toxicity associated with furan exposure in both animals and humans has been documented. Protocatechuic acid (PCA), a dietary polyphenolic chemical, reportedly elicits beneficial effects on the male reproductive system. However, the influence of PCA on the reproductive toxicity related to furan exposure is unavailable in the literature. The current study evaluated the effects of PCA on the dysfunctional reproductive axis caused by furan exposure in rats. Experimental animals were exposed to furan (8 mg/kg) or co-treated with furan (8 mg/kg) and PCA (25 or 50 mg/kg) for twenty-eight successive days. Results revealed that PCA treatment significantly alleviated furan-mediated declines in sperm production and characteristic qualities as well as in serum levels of prolactin, luteinizing hormone, follicle-stimulating hormone, and testosterone. Further, PCA attenuated furan-induced reduction in antioxidant enzyme activities and testicular function marker enzymes, namely lactate dehydrogenase, glucose-6-phosphate dehydrogenase, acid phosphatase, and alkaline phospha- tase. PCA effectively mitigated furan-mediated increases in myeloperoxidase activity, levels of reactive oxygen and nitrogen species, nitric oxide, tumour necrosis factor-alpha, and interleukin-1^ in testes, epididymis, and hypothalamus of rats. Moreover, PCA increased anti-inflammatory cytokine interleukin-10 but suppressed cas- pase-9 and caspase-3 activities and ameliorated injuries in the testes, epididymis, and hypothalamus of furan- treated rats. In conclusion, PCA ameliorated deficits in the hypothalamic-pituitary-gonadal axis function in furan-exposed rats by suppressing oxido-inflammatory stress and apoptosis.Item Protocatechuic acid ameliorates neurobehavioral defìcits via suppression of H) oxidative damage, inflammation, caspase-3 and acetylcholinesterase activities in diabetic rats(Elsevier Ltd., 2019) Adedara, I. A. || || || ||; Fasina, O. B.; Ayeni, M. F.; Ajayi, O. M.; Farombi, E. O.Clinical and experimental data have demonstrated that diabetes is associated with neurological complications. Protocatechuic acid (PCA) is a phenolic phytochemical widely reported to possess antidiabetic property. However, there is no scientific information on the influence of PCA on diabetes-induced neurotoxicity. The present study aimed at investigating the neuroprotective mechanism of PCA in streptozotozin (STZ)-induced type 1 diabetic rats orally treated with PCA (50 mg/kg body weight) or glibenclamide (5 mg/kg body weight) for 45 consecutive days. Locomotor behavior was analyzed using video-tracking software during the 8-min trial in a novel environment whereas the pancreas, cerebrum and cerebellum of the rats were processed for biochemical analyses. Results showed that treatment of diabetic rats with PCA at 50 mg/kg significantly (p < 0.05) im- proved the locomotor and motor activities including the average speed, total time mobile, distance travelled, body rotation, turn angle, forelimb grip and grooming when compared with untreated diabetic rats. Moreover, the prevention of diabetes-mediated increase in acetylcholinesterase activity, biomarkers of inflammatory and oxidative stress as well as caspase 3 activity by PCA treatment was accompanied by improved pancreatic, cer- ebral and cerebellar architectures. Collectively, the neuroprotective mechanisms of PCA is related to its anti- oxidant, anti-inflammatory and anti-apoptotic activities.Item 6-Gingerol abates benzo[a]pyrene-induced colonic injury via suppression of oxido-inflammatory stress responses in BALB/c mice(Elsevier B.V., 2019) Ajayi, B. O. || ||; Adedara, I. A.; Farombi, E. O.Exposure to benzo[a]pyrene (BaP), the most toxic polycyclic aromatic hydrocarbon and a procarcinogen, is a global health concern which necessitates preventive measures. [6]-Gingerol (6-G), the most pharmacologically active constituent of ginger has been reported to promote gut health in various experimental settings. This study investigated the role of 6-G in BaP-induced colonic oxidative and inflammatory stress responses in mice. Experimental mice were randomly assigned into five groups of eight mice each and were orally gavage with BaP (125 mg/kg) singly or in combination with 6-G at 50 and 100 mg/kg for 14 consecutive days. Following sacrifice, the colonic activities of superoxide dismutase (SOD), catalase (CAT), glutathione S-transferase (GST), myeloperoxidase (MPO) as well as levels of glutathione (GSH), nitrites and lipid peroxidation (LPO) were assessed spectrophotometrically. Moreover, colonic concentration of epoxide hydrolase (EPXH), tumor necrosis factor alpha (TNF-α), interleukin-1 β (IL-1β), cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS) were assessed using ELISA. Administration of 6-G augmented BaP detoxification and colonic antioxidant status by increasing the EPXH, GST, SOD and CAT activities, GSH level with concomitant decrease in MDA level when compared with BaP alone group. In addition, 6-G suppressed BaP-induced colonic inflammation by decreasing MPO activity as well as nitrites, TNF-α, IL-1β, COX-2 and iNOS levels when compared with BaP alone group. In conclusion, 6-G protected against a decrease in colonic epoxide detoxifying enzymes and antioxidant defense mechanisms caused by BaP.Item Dietary protocatechuic acid abrogates male reproductive dysfunction in streptozotocin-induced diabetic rats via suppression of oxidative damage, inflammation and caspase-3 activity(Elsevier B.V., 2019) Adedara, I. A. || || || || ||; Okpara, E. S.; Busari, E. O.; Omole, O.; Owumi, S. E.; Farombi, E. O.Clinical and experimental studies demonstrated that reproductive dysfunction is a non-lethal complication of diabetes. Protocatechuic acid (PCA) reportedly elicited several pharmacological effects in diabetic animals. However, there is paucity of information on the role of PCA in reproductive dysfunction associated with diabetes. The present study investigated the influence of PCA on the functional changes along the hypothalamicpituitary-testicular axis in male diabetic rats. Streptozotocin (STZ)-induced diabetic rats were orally treated with PCA at 25 and 50 mg/kg body weight for 45 consecutive days. Results showed that PCA treatment significantly dwindled blood glucose level as well as prevented diabetes mediated decrease in body weight gain and organosomatic indices of the testes and epididymis in the treated rats. Moreover, PCA increased the reproductive hormone levels, marker enzymes of testicular function and sperm functional characteristics in the treated rats. Further, PCA augmented the antioxidant status, inhibited lipid peroxidation and suppressed pro-inflammatory biomarkers including myeloperoxidase (MPO) activity, nitric oxide (NO) and tumor necrosis factor alpha (TNF-α) levels as well as caspase-3 activity inhypothalamus, testes and epididymis of diabetic rats. Collectively, PCA effectively abrogated reproductive deficits in diabetic rats via mechanisms involving suppression of oxidative stress, inflammation and caspase-3 activity along with enhancement of sperm functional parameters. Thus, PCA may preserve reproductive health in humans suffering from diabetes.Item Ethanol exacerbates manganese - induced functional alterations along the hypothalamic-pituitary-gonadal axis of male rats(Elsevier B.V., 2018) Nkpaaa, K. W.; Amadi, B. A.; Adedara, I. A; Wegwu, M. O.; Farombi, E. O.Manganese (Mn) exposure has been reported to induce reproductive dysfunction in animal and humans. Studies have shown that a large percentage of adolescent and adult populations tend to consume alcohol in a binge pattern. However, there is no information on the influence of alcohol on Mn - induced functional alteration along the hypothalamic - pituitary - gonadal axis. This study aimed to evaluate the influence of ethanol (EtOH) on Mn - induced functional alteration along the hypothalamic - pituitary - gonadal axis. Rats were exposed to Mn alone at 30 mg/kg body weight or co-expose with EtOH at 1.25 and 5 g/kg body weight for 35 consecutive days. Results showed that EtOH exposure significantly (p < 0.05) exacerbated Mn - induced decrease in anti- oxidant enzymes activities, glutathione level and increased oxidative stress biomarkers in the hypothalamus, testes an epididymis of the exposed rats. Moreover, induction of inflammation was associated with disruption of histo-architecture of the hypothalamus, testes and epididymis of rats treated with Mn alone, EtOH alone or in combination. Furthermore, EtOH significantly exacerbated Mn - induced diminution in reproductive hormones and marker enzymes of testicular functions coupled with decreased sperm quantity and quality. Taken together, EtOH exacerbates Mn - induced functional alteration along the hypothalamic - pituitary - gonadal axis in rats via mechanisms involving induction of oxidative/nitrosative stress, lipid peroxidation and inflammation in rats.Item Benzo(a)pyrene induces oxidative stress, pro-inflammatory cytokines, expression of nuclear factor-kappa B and deregulation of wnt/beta- catenin signaling in colons of BALB/c mice201(Elsevier Ltd., 2016) Ajayi, B. O.; Adedara, I. A.; Farombi, E. O.The incidence of colonic toxicity has been epidemiologically linked to the consumption of foods contaminated with benzo[a]pyrene (B[a]P). The present study investigated the effects of B[a]P on biomarkers of colonic stress, inflammation and Wnt/β-catenin signaling in colon of BALB/c mice. B[a]P was administered orally at 62.5, 125 and 250 mg/kg of B[a]P for 7 days by oral gavage. Exposure to B[a]P significantly decreased the colonic antioxidant enzyme activities and glutathione levels with concomitant significant increase in myeloperoxidase activity, nitric oxide and lipid peroxidation levels. Colon histopathology results showed treatment-related lesions characterized by atrophy, mucosal ulceration and gland erosion in the B[a]P-treated mice. Immunohistochemistry analysis showed that B[a]P treatment increased the protein expression of nuclear factor kappa B, pro-inflammatory cytokines namely tumor necrosis factor alpha and interleukin-1β, as well as cyclooxygenase-2 and inducible nitric oxide synthase in the mice colon. Altered canonical Wnt signaling was confirmed using diaminobenzidine staining for p38 mitogen activated protein kinase, β-catenin expression and absence of adenomatous polyposis coli following B[a]P administration. The present data highlight that exposure to B[a]P induces colonic injury via induction of oxidative and nitrosative stress, inflammatory biomarkers and dysregulation of Wnt/β-catenin signaling, thus confirming the role of B[a]P in the pathogenesis of colonic toxicity.