Biochemical investigation into the influence of telfairia occidentalis on hepatic oxidative stress markers and pro-inflammatory biomarkers induced by streptozotocin

Abstract

In rat models of diabetes, this research examined the biochemical impact of Telfairia occidentalis (TO) on pro-inflammatory biomarkers and hepatic oxidative stress markers caused by streptozotocin (STZ). There were five experimental groups: G 1 (Normal control) received 0.5 ml of distilled water; G 2 through 5 received 10% fructose for 14 days, after which STZ was administered intraperitoneally once. After the diagnosis of diabetes was confirmed, rats in groups 3 (TO1), 4 (TO2), and 5 (MET) were given 200 mg/kg b.w. TO, 300 mg/kg b.w. TO, and 300 mg/kg b.w. Metformin, respectively, for 28 days. The findings show that STZ significantly (p<0.05) increased malondialdehyde (MDA) levels in diabetic rats relative to the control group and significantly (p<0.05) decreased the activities of liver antioxidant enzymes such as catalase (CAT), reduced glutathione (GSH), glutathione S-transferase (GST), glutathione peroxidase (GPx), and superoxide dismutase (SOD). On the other hand, administration of TO (200 mg/kg and 300 mg/kg) and Metformin (300 mg/kg) resulted in a significant (p<0.05) increase in antioxidant enzyme activities and a significant (p<0.05) decrease in MDA levels. Furthermore, the inflammatory biomarkers myeloperoxidase (MPO), interleukin-1beta (IL-1β), tumor necrosis factor-alpha (TNF-α), inducible nitric oxide synthase (iNOS), and cyclooxygenase-2 (COX-2) as well as the apoptotic marker caspase-3 were significantly (p<0.05) elevated upon STZ induction; however, these elevations were significantly (p<0.05) attenuated upon TO administration, mirroring the effects of Metformin. In conclusion, Telfairia occidentalis significantly reduces the oxidative stress markers, inflammatory reactions brought on by STZ, and liver antioxidant status in diabetic rats. These results point to TO's possible therapeutic benefit in reducing diabetes-related liver problems via regulating oxidative and inflammatory pathways.