Aloin attenuates cognitive impairment and inflammation induced by d-galactose via down-regulating ERK, p38 and NF-κB signaling pathway.

Abstract

Oxidative stress is considered as major culprit for neurodegenerative diseases and triggers cognitive and memory impairments. The present study mainly aimed to study the protective effects and underlying mechanisms of aloin on d-galactose (d-gal) induced ageing mice. Our results demonstrated that chronic administration of d-gal (150 mg kg-1) in mice caused spontaneous and cognitive impairments, as determined by open-field test and Morris water-maze test. Aloin treatment significantly ameliorated histopathological damage, attenuated the microglia activation and reduced levels of inflammatory mediators, such as tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β) and IL-6 in the hippocampus. Moreover, it effectively suppressed the level of reactive oxygen species (ROS) and increased antioxidant enzymes activities. Further data showed that these protective effects were accompanied by inhibition of the activation of nuclear factor kappa B and the phosphorylation of p38 and ERK. In conclusion, the present study suggests that aloin can ameliorate d-gal induced oxidative stress, cognitive impairment and inflammation, possibly via mediating the ERK, p38 and NF-κB signaling pathways.

• Authors: Junjie Zhong, Fan Wang, Zhifu Wang, Chao Shen, Yongtao Zheng, Fukai Ma, Tongming Zhu, Luping Chen, Qisheng Tang, Jianhong Zhu
• Journal: International immunopharmacology (Int Immunopharmacol) Vol. 72 Pg. 48-54 (Jul 2019) ISSN: 1878-1705 [Electronic] Netherlands
• PMID: 30959371 (Publication Type: Journal Article)
• Copyright: Copyright © 2019 Elsevier B.V. All rights reserved.

Chemical References

• Cytokines
• NF-kappa B
• Neuroprotective Agents
• Superoxide Dismutase
• Glutathione
• Emodin
• alloin
• Galactose

Topics

• Animals
• Brain (drug effects, metabolism, pathology)
• Cognitive Dysfunction (chemically induced, drug therapy, metabolism, pathology)
• Cytokines (metabolism)
• Down-Regulation (drug effects)
• Emodin (analogs & derivatives, pharmacology, therapeutic use)
• Galactose
• Glutathione (metabolism)
• MAP Kinase Signaling System (drug effects)
• Male
• Maze Learning (drug effects)
• Mice, Inbred C57BL
• NF-kappa B (metabolism)
• Neuroprotective Agents (pharmacology, therapeutic use)
• Oxidative Stress (drug effects)
• Superoxide Dismutase (metabolism)