Oleuropein, a phenolic component of Olea europaea L. ameliorates CCl4-induced liver injury in rats through the regulation of oxidative stress and inflammation.

OBJECTIVE: This study aimed to assess the hepatoprotective role of oleuropein (Olp), a phenolic compound found in olive, against carbon tetrachloride (CCl4)-induced liver damage in rats. MATERIALS AND METHODS: The research involved male albino rats, which received intraperitoneal injections of 100 mg/kg b.w. of oleuropein for 8 consecutive weeks before being subjected to carbon tetrachloride (CCl4) at a dosage of 1.0 ml/kg b.w. Changes induced by CCl4 in antioxidant and inflammatory marker levels were assessed using ELISA assay kits. Moreover, CCl4-induced liver tissue architecture alteration, fibrosis, and expression pattern of protein were evaluated by performing H&E, Sirius red, Masson trichrome, and immunohistochemistry staining. RESULTS: Increased serum transaminases and massive hepatic damage were observed by this liver toxicant. The hepatic injury was further evidenced by a significant decrease in antioxidant enzyme activity [superoxide dismutase (SOD), glutathione peroxidase (GPx), Glutathione (GSH) and Total Antioxidant Capacity (T-AOC)]. The administration of CCl4 resulted in an increased inflammatory response, which was measured by C-reactive protein, interleukin-6, as well as tumor necrosis factor-alpha. Olp as a curative regimen led to significant attenuation in the inflammatory response and oxidative/nitrosative stress. This polyphenol treatment improved the hepatic tissue architecture and decreased fibrosis. In the CCl4 treatment group, the expression pattern of IL-6 protein was high, whereas expression was decreased after Olp, as evidenced by immunohistochemistry staining. CONCLUSIONS: The study suggests that oleuropein treatment has the potential to reduce liver damage caused by CCl4 induction by inhibiting oxidative stress and inflammation and maintaining liver tissue architecture. This could make it a promising treatment option for liver pathogenesis.

Oral administration of naringenin and a mixture of coconut water and Arabic gum attenuate oxidative stress and lipid peroxidation in gentamicin-induced nephrotoxicity in rats.

OBJECTIVE: This study aimed to investigate the effect of oral administration of naringenin in combination with an aqueous mixture of coconut water (CW) and Arabic gum (AG) on renal function, lipid profile, antioxidant activity, and morphology in gentamicin-induced kidney injury in rats. MATERIALS AND METHODS: Forty adult male Wistar rats were equally divided into four groups. 1-Negative control group, 2-positive control group (Gentamicin), 3-Naringenin+AG+CW, 4-Gentamicin+Naringenin+AG+CW: groups 2 and 4 were treated with gentamicin. After six weeks, the rats were anesthetized with diethyl ether, and blood was collected by cardiac puncture and dissected to collect the kidneys. Biochemical studies were performed to determine the levels of urea, creatinine, lipids, total antioxidant capacity, and lipid peroxide, antioxidant enzyme activity in the kidney, total phenolic content (TPC), radical-scavenging activity, calcium, magnesium, and potassium in AG, CW, and their mixture. Also, kidney histopathology was performed. RESULTS: Renal injury manifests as elevated serum urea and creatinine levels. A significant increase in total cholesterol, triglycerides (TG), low-density lipoprotein cholesterol (LDL-C), and malondialdehyde (MDA) was also noted. The activities of antioxidant capacity (TAC) and reduced glutathione (GSH) significantly decreased in the serum. There was a reduction in the activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and catalase (CAT) activities in kidney homogenates. Gentamicin administration induces morphological changes in the kidneys. Oral administration of naringenin+AG+CW significantly overturned all of the above-mentioned abnormalities. CONCLUSIONS: These results show that the naringenin+AG+CW combination exhibited an additive effect against renal dysfunction and structural damage through antioxidant and anti-inflammatory mechanisms, as well as replenishing and balancing intracellular and extracellular electrolytes. Therefore, oral administration of these three ingredients could potentially provide better protection and serve as a unique therapeutic tool against nephrotoxicity caused by gentamicin.