氧化应激
甘草甜素
神经保护
药理学
炎症
HMGB1
神经毒性
细胞凋亡
TLR4型
化学
神经退行性变
KEAP1型
NF-κB
医学
毒性
内科学
生物化学
疾病
基因
转录因子
作者
Abdallah M. Gendy,Hagar M. El-Sadek,Mohamed M. Amin,Kawkab A. Ahmed,Mohamed Kotb El-Sayed,Alaadin E. El-Haddad,Ayman A. Soubh
出处
期刊:Life Sciences
[Elsevier]
日期:2023-02-01
卷期号:314: 121317-121317
被引量:4
标识
DOI:10.1016/j.lfs.2022.121317
摘要
Glycyrrhizin (Glyc) is a saponin triterpenoid that has signified its efficacy against Huntington's disease (HD). Nonetheless, its mechanism has not been fully clarified. Accordingly, this study was designed to evaluate the plausible mechanism of action of Glyc against 3-nitropropionic acid (3-NP)-induced HD.Rats were treated with Glyc (50 mg/kg, i.p.) for 3 weeks and 3-NP (10 mg/kg, i.p.) was administered at the latter 2 weeks alongside to induce HD.Animals exposed to 3-NP revealed a reduction in body weight, neurobehavioral abnormalities, and various deleterious effects related to overexpression of HMGB1 such as oxidative stress, apoptosis, and inflammation. Promisingly, Glyc administration provided valuable effects by reversing the decline in body weight with improved neurobehavioral deficits. Ameliorating oxidative stress via restoring GSH, SOD, and Nrf2 alongside with MDA suppression was evident. Furthermore, Glyc switched the HMGB1/TLR4/NF-κB p65 signaling off, reduced IL-6, IL-β, TNF-α, caspase-3, and increased Bcl-2 as well as BDNF. All these beneficial effects were mirrored by a better histopathological picture upon using Glyc that suppressed gliosis by reducing GFAP expression as observed in the immunohistochemistry results.Accordingly, the current study demonstrated a promising neuroprotective effect of Glyc against experimentally induced HD through alleviating deleterious events by diverse mechanisms.
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