RESUMO
Background of the Study: The increase in the therapeutic use of tramadol in the management of moderate to severe pains in some disease conditions and its unregulated access has led to its associated toxicity and there is little or no information on the protection against its associated toxicity. Aim of the Study: Considering the medicinal value of pumpkin seed oil, its availability, and neglected use, it becomes necessary to evaluate the possible potential of the seed oil in tramadol-induced oxidative stress in Wister Albino rats. Methods of the Study: This study used fifty-six (56) albino rats to determine the impact of Cucurbita pepo seed oil (CPSO) on tramadol-induced oxidative stress. The rats were grouped into 7. After a week of acclimatization, rats in group 1 (normal control) had access to water and food, while rats in group 2 received 5 mL/Kg (b.w) of normal saline. 100 mg/kg of tramadol (TM) was delivered to groups 3-6 to induce toxicity. The third group (TM control) received no treatment, whilst the other 3 groups (TM-CPSO treatment groups) received 5, 2.5, and 1.5 mL/Kg of CPSO, respectively. Group 7 received only 5 mL/kg CPSO (CPSO group). Similarly, groups 2 through 7 had unrestricted access to food and water for 42 days and received treatments via oral intubation once per day. Indicators of oxidative stress were discovered in the brain homogenate. Results: TM toxicity was demonstrated by a considerable increase (P < .05) in the brain MDA level and a significant drop (P < .05) in the brain GSH level, as well as a significant reduction (P < .05) in GPx, catalase, SOD, GST, and quinone reductase activities. Conclusion: The dose-dependent delivery of CPSO was able to restore not only the activity but also the concentrations of the altered markers.
RESUMO
This study demonstrated the therapeutic potentials of Cucumeropsis mannii seed oil (CMSO) capable of alleviating BPA-induced dyslipidemia and adipokine dysfunction. In this study, we evaluated the effects of CMSO on adipokine dysfunctions and dyslipidemia in bisphenol-A (BPA)-induced male Wistar rats. Six-week-old 36 albino rats of 100-200 g weight were assigned randomly to six groups, which received varied doses of BPA and/or CMSO. The administration of BPA and CMSO was done at the same time for 42 days by oral intubation. The adipokine levels and lipid profile were measured in adipose tissue and plasma using standard methods. BPA induced significant (p < .05) increases in triglycerides, cholesterol, leptin, LDL-C, and atherogenic and coronary risk indices in adipose tissue and plasma, as well as a decrease in adiponectin and HDL-C levels in Group II animals. BPA administration significantly (p < .05) elevated Leptin levels and reduced adiponectin levels. BPA plus CMSO reduced triglycerides, cholesterol, leptin, LDL-C, and atherogenic and coronary risk indices while increasing adiponectin levels and HDL-C in adipose tissue and plasma (p < .05). The results showed that BPA exposure increased adipose tissue as well as serum levels of the atherogenic index, triglycerides, cholesterol, coronary risk index, LDL-C, leptin, and body weight with decreased adiponectin levels and HDL-C. Treatment with CMSO reduced the toxicities caused by BPA in rats by modulating the body weight, adiponectin/leptin levels, and lipid profiles in serum and adipose tissue. This study has shown that CMSO ameliorates BPA-induced dyslipidemia and adipokine dysfunctions. We suggest for further clinical trial to establish the clinical applications.