Cellgevity® attenuates liver distruption, oxidative stress and inflammation in STZ-diabetic male rats

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dc.contributor.authorOgunlabi OO
dc.contributor.authorAdegbesan BO
dc.contributor.authorEzima EN
dc.contributor.authorAdebisi AA
dc.date.accessioned2022-07-25T22:17:48Z
dc.date.available2022-07-25T22:17:48Z
dc.date.issued2021
dc.descriptionScientific African
dc.description.abstractThe imbalance between reactive oxygen species (ROS) production and the innate antioxidant defence promotes oxidative distress and contributes to tissue dysfunctions which are the hallmark of diabetic complications. Diabetic hepatic injury is less reported, yet it is a target organ damage condition related to diabetes. This study investigated the hepato-protective potentials of Cellgevity® in Streptozotocin (STZ)-diabetic male rats. The rats were assigned into – Control group and diabetes induced groups (DM-untreated, DM-treated 1 and DM-treated 2 groups respectively). Separate treatment of the DM-treated 1 and DM-treated 2 groups with therapeutic doses of Cellgevity® (25 mg/kg and 40 mg/kg BW respectively) was conducted for 30 days, while the control and DM-untreated groups receieved oral distilled water (placebo). The animals were then sacrificed and their sera were evaluated for total antioxidant status and biomarkers of hepatic function. The rats’ liver homogenates were also evaluated for inflammation, nitric oxide, lipid peroxidation and antioxidant enzymes activity. Treatment with Cellgevity® significantly increased the serum total antioxidant status (2 fold) and it reduced the serum ALT, AST, ALP and bilirubin levels compared to untreated diabetes by at least 1.4 fold. Hepatic activities of glutathione peroxidase (GPx), superoxide dismutase (SOD), and catalase (CAT) were significantly increased by over 130%, while liver TNF-α, nitrite and MDA levels were reduced by over 140% compared to the diabetic untreated group. The results present promising evidence for the therapeutic potential of Cellgevity® against diabetes-induced liver dysfunction, which might be through the modulation of ROS and inflammation production respectively.
dc.identifier.citation10.1016/j.sciaf.2021.e01055
dc.identifier.issn2468-2276
dc.identifier.urihttps://nerd.ethesis.ng/handle/123456789/238
dc.language.isoen
dc.subjectSTZ-diabetes
dc.subjectLiver function
dc.subjectHepatopathy
dc.subjectOxidative stress
dc.subjectInflammation
dc.subjectAntioxidant enzymes
dc.subjectCellgevity®
dc.titleCellgevity® attenuates liver distruption, oxidative stress and inflammation in STZ-diabetic male rats
dc.typeArticle
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