Hesperidin protects against aluminum-induced renal injury in rats via modulating MMP-9 and apoptosis: biochemical, histological, and ultrastructural study.

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.

Crocin averts functional and structural rat hepatic disturbances induced by copper oxide nanoparticles.

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.

Impact of cisplatin administration on cerebellar cortical structure and locomotor activity of infantile and juvenile albino rats: the role of oxidative stress.

The central neurotoxicity of cisplatin (CisPt) has always raised questions especially during development, but few studies are available. Hence, this work was designed to assess the CisPt's impacts on the postnatal rat cerebellum via evaluation of locomotor activity, histological and immunohistochemical studies, and to focus on cerebellar oxidative stress-related alterations. Eighty newborn pups were divided into 2 equal experimental groups: the control group was kept without any treatment and CisPt-treated group received a single subcutaneous injection of CisPt (5 µg /g b.w.) in their nape at PD10. Ten rats at PD11, PD17, and PD30 ages were weighed, then deeply anesthetized and sacrificed. For locomotor assessment, 20 pups were divided equally into control and CisPt-treated groups and tested at PD11-13, PD15-17, and PD28-30 ages. CisPt-treated rats suffered from decreased motor activity and showed decreased body and cerebellar weights, reduced levels of enzymatic antioxidants (SOD and CAT), and non-enzymatic antioxidant defense (GSH), and increase of lipid peroxidation marker (MDA). Histopathologically, CisPt sowed deleterious changes within cerebellar cortical layers in the form of vacuolations, decreased thickness, and hemorrhage (in PD17), while Purkinje cells exhibited profound degenerative changes in the form of swelling, disrupted arrangement, distortion, and nuclear shrinkage. In CisPt-treated rats, GFAP demonstrated upregulated, hypertrophied, and branched Bergmann glial fibers and reactive astrogliosis. Immuno-localization of Ki-67-positive cells revealed defective migration associated with decreased proliferation in early ages in addition to glial proliferation in PD30. In conclusion, CisPt causes oxidative stress-related deleterious effects on structure of developing cerebellar cortex and affects locomotor activity.