Nanoparticles Mitigate Aging-Related Oxidative Injured Brain Induced by D-galactose In Rats Through Antioxidants, Anti-Inflammatory, and MAPK Pathways

Overview

Journal Int J Nanomedicine

Publisher Dove Medical Press

Specialty Biotechnology

Date 2023 Oct 9

PMID 37808455

Authors

Heba I Ghamry

Mustafa Shukry

Mohamed A Kassab

Foad A Farrag

Nagi M El-Shafai

Enas Elgendy

Amany N Ibrahim

Salwa A Elgendy

Ali Behairy

Samah F Ibrahim

Florin Imbrea

Crista Florin

Mohamed Abdo

Inas A Ahmed

Marwa H Muhammad

Hala Anwer

Ahmed Abdeen

Affiliations

Soon will be listed here.

Abstract

Background: Loss of normal function is an inevitable effect of aging. Several factors contribute to the aging process, including cellular senescence and oxidative stress.

Methods: We investigate how Nanoparticles (NSP) protect against aging injury induced by d-galactose (D-gal) in the rat. So, we subcutaneously (S/C) injected D-gal at 200 mg/kg BW to see if Arthrospira platensis Nanoparticles (NSP) might protect against the oxidative changes generated by D-gal. NSP (0.5 mg/kg body weight once daily by gastric gavage) was given to all groups apart from the control and D-gal groups. The d-gal + NSP group was supplemented with 200 mg of D-gal per kg BW once a day and NSP 0.5 mg/kg BW given orally for 45 days. Biochemical, mRNA expression, and histological investigations of brain tissues were used to evaluate the oxidative alterations caused by d-gal and the protective role of NSP.

Results: Our data demonstrated that d-gal was causing significant reductions in relative brain and body weight with increased malondialdehyde (MDA) and redox oxygen species (ROS) levels and increases in serum creatine phosphokinase (CPK) and creatine phosphokinase isoenzyme BB (CPK-BB) with marked decreases in the level of antioxidant enzyme activity in the brain and acetylcholinesterase activity augmented with a phosphorylated H2A histone family member X (γ-H2AX) level increased. The D-gal group had considerably higher phosphorylated p38 mitogen-activated protein kinases (P38MAPK) and C-Jun N-terminal (JNK) kinases. The d-gal administration stimulates the apoptotic gene expression by downregulating the brain superoxide dismutase (SOD), catalase (CAT), and nuclear factor erythroid 2-related factor 2 (Nrf2). The NSP administration saved these parameters in the direction of the control. The brain histopathologic and immunohistochemistry analysis findings support our findings on NSP's protective role.

Conclusion: The NSP may be a promising natural protective compound that can prevent aging and preserve health.

Citing Articles

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