Calcium dobesilate protects against d‐galactose‐induced hepatic and renal dysfunction, oxidative stress, and pathological damage

Abstract

Calcium dobesilate (CaD) is used for the treatment of diabetic retinopathy and nephropathy. This agent exerts antioxidant effects. In the present study, we evaluated the protective effects of oral administration of CaD against hepatorenal damages in a mice model of aging induced by D-galactose (Dgal). We used 28 male albino mice, which equally and randomly were divided into four groups as follows: intact, aging (D-gal at the dose of 500 mg/kg, p.o.), aging + CaD 50 (D-gal plus CaD at the dose of 50 mg/kg), and aging + CaD 100 (D-gal plus CaD at the dose of 100 mg/kg, p.o.). All drugs were administered orally once a day for 42 days. The liver and kidney damages were evaluated by measuring mass indices, levels of serum creatinine and blood urea nitrogen, and activities of serum alanine aminotransferase, aspartate aminotransferase, and alkaline phosphatase and by histopathological evaluation. Moreover, hepatic and renal tissue oxidant/ antioxidant markers (malondialdehyde, superoxide dismutase, catalase, and glutathione peroxidase) were measured. The results showed that D-gal treatment induced significant oxidative stress in the kidney and liver that was paralleled by dysfunctions and histological alterations of these organs. CaD significantly improved the liver and kidney indices, implemented functional capacity of the liver and kidney, as well as decreased oxidative stress

A comprehensive view on the quercetin impact on bladder cancer: Focusing on oxidative stress, cellular, and molecular mechanisms

“…Quercetin, an efficient ROS scavenger, inhibits oxidative stress and damage by reducing ROS and blocking lipid peroxidation, which is associated with the oxidation of its catechol and OH groups at C3. Furthermore, to enhance quercetin's antioxidative properties, it was proposed to recombine it with some metal or complex ions [56,57]. Quercetin promotes the expression level of antioxidant enzymes such as GPX1, catalase (CAT), and SOD1 in addition to suppression of major oxidative enzymes such as acetylcholinesterase (AChE) and butyrylcholinesterase (BChE) [58].…”

Distinct signatures on d‐galactose‐induced aging and preventive/protective potency of two low‐dose vitamin D supplementation regimens on working memory, muscular damage, cardiac and cerebral oxidative stress, and SIRT1 and calstabin2 downregulation

“…At the experimental level, the study of natural aging in specimens confronts several intrinsic limitations, such as individual heterogeneity, comorbidities, and survival, but also extrinsic research constraints related to costly and time‐consuming approaches which can be minimized using models for accelerated aging. A well‐accepted experimental model of oxidative stress‐related physiological aging is the long‐term treatment of mice with d ‐galactose ( d ‐gal) (Azman & Zakaria, 2019 ; Hakimizadeh, Zamanian, Borisov, et al, 2022 ; Hakimizadeh, Zamanian, Damankhorshid, et al, 2022 ). Chronic exposure to this reducing sugar accelerates aging through increased generation of reactive oxygen species (ROS) oxidative stress and antioxidant enzyme downregulation (Anand et al, 2012 ).…”