No abstract

Aluminum, one of the most abundant metallic elements, is known to be toxic to multiple organs including the kidneys. This study aimed to investigate the pleiotropic nephroprotective effects of Hesperidin in aluminum chloride (ALCL3)-induced renal injury, highlighting the potential molecular mechanisms underlying. Twenty-four male albino rats were divided into four groups: control, Hesperidin (80 mg/kg BW, orally), ALCL3 (10 mg/kg BW, IP), and ALCL3 + Hesperidin groups. By the end of the study, blood samples were collected, and tissue samples were harvested at sacrifice. ALCL3 rats showed dramatically declined renal function, enhanced intrarenal oxidative stress, inflammation, apoptosis, and extravagant renal histopathological damage with interstitial fibrosis as shown by a higher Endothelial, Glomerular, Tubular, and Interstitial (EGTI) score. Hesperidin significantly reversed all the aforementioned detrimental effects in ALCL3-treated rats. The study verified the nephroprotective effects of Hesperidin on ALCL3-induced renal damage and confirmed the critical role of extracellular matrix (ECM) remodeling and apoptosis inhibition. Graphical Abstract

No abstract

Background Exposure to nanoparticles became inevitable in our daily life due to their huge industrial uses. Copper oxide nanoparticles (CuONPs) are one of the most frequently utilized metal nanoparticles in numerous applications. Crocin (CRO) is a major active constituent in saffron having anti-inflammatory and antioxidant potentials. Objectives We designed this study to explore the probable defensive role of CRO against CuONPs-induced rat hepatic damage. Materials and methods Therefore, 24 adult rats were randomly distributed into 4 equal groups as negative control, CRO, CuONPs, and co-treated CuONPs with CRO groups. All treatments were administered for 14 days. The hepatotoxic effect of CuONPs was evaluated by estimation of hepatic alanine aminotransferase and aspartate aminotransferase enzymes, hepatic oxidative malondialdehyde and antioxidant glutathione reduced, serum levels of inflammatory biomarkers (tumor necrosis factor-alpha, interleukin-1-beta, and nuclear factor kappa B), and expression of the apoptotic BAX in hepatic tissues; in addition, histopathological examination of the hepatic tissues was conducted. Results We found that concurrent CRO supplement to CuONPs-treated rats significantly averted functional and structural rat hepatic damage as documented by decreased hepatic enzymes activities, restored hepatic oxidant/antioxidant balance, decreased serum levels of inflammatory biomarkers, reversed BAX-mediated apoptotic cell death in hepatic tissues along with repair of CuONPs-induced massive hepatic structural and ultrastructural alterations. Conclusions It is concluded that combined CRO supplement to CuONPs-treated rats improved hepatic function and structure by, at least in part, antioxidant, anti-inflammatory, and antiapoptotic mechanisms.

No abstract