L-Ascorbic Acid and Curcumin Prevents Brain Damage Induced via Lead Acetate in Rats: Possible Mechanisms

Abstract

Lead acetate (lead ac.) is a widespread ecological toxicant that can cause marked neurotoxicity and decline in brain functions. This study aimed to evaluate the possible neuroprotective role of L-ascorbic (ASCR) and curcumin (CRCM) alone or together against lead ac.-induced neurotoxicity. Rats were injected with lead ac. then treated orally with ASCR and CRCM alone or in combination for seven days. Lead ac. caused elevation in brain tumor necrosis factor- α (TNF-α), interleukin-6 (IL-6), caspase-3, and malondialdehyde (MDA) levels, while superoxide dismutase (SOD), reduced glutathione (GSH) as well as the expression of brain-derived neurotrophic factor (BDNF), cAMP response element-binding (CREB) and Beclin1 were down-regulated. Expressions of C/EBP homologous protein (CHOP) and mammalian Target of rapamycin kinase (mTOR) were upregulated in brain tissues matched with the control group. Histopathological examination supported the previously mentioned parameters, the administration of the antioxidants in question modulated all the altered previous parameters. The combination regimen achieved the superlative results in the antagonizing lead ac.-induced neurotoxicity via its antioxidant and anti-apoptotic activities.

Antioxidative and Anti-Inflammatory Activity of Ascorbic Acid

“…As a result, the levels of pro-inflammatory factors in cells are lowered. It has been described that ascorbate (500 mg/day) significantly reduces IL-6 and TNF-α levels in brain tissue [ 138 ] and inhibits IL-6 protein release from a contracting skeletal muscle [ 139 ]. Moreover, ascorbic acid significantly downregulates the expression of pro-inflammatory factors (IL-6, IL-12, and TNF-α) and upregulates anti-inflammatory cytokines (IL-4 and IL-10) [ 140 ] in mouse splenocytes.…”

Regular combined training and vitamins modulated the apoptosis process in diabetic rats: Bioinformatics analysis of heart failure's differential genes expression network correlated with anti‐apoptotic process

“…Hence, ascorbic acid consumption could inhibit apoptosis in the hippocampus of diabetic rats by regulating Bcl2 and Bax expression. Based on these studies, the antioxidant properties of ascorbic acid prevented the apoptosis process (Alhusaini et al, 2022; Hsueh et al, 2020; JafariAnarkooli et al, 2007; Marik, 2018; Nam et al, 2018; Vineetha et al, 2018). Therefore, it could be concluded that antioxidant supplementation might eliminate free radicals and improve the antioxidant defense system's ability, leading to apoptosis inhibition.…”

“…Hence, ascorbic acid consumption could inhibit apoptosis in the hippocampus of diabetic rats by regulating Bcl2 and Bax expression. Based on these studies, the antioxidant properties of ascorbic acid prevented the apoptosis process (Alhusaini et al, 2022;Hsueh et al, 2020;JafariAnarkooli et al, 2007;Marik, 2018;Nam et al, 2018;Vineetha et al, 2018).…”