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¹Department of Physiology, Baicheng Medical College, Baicheng, 137000 Jilin, China.

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Summary

This summary is machine-generated.

Genistein (Gen) protects aging rat neurons by inhibiting endoplasmic reticulum stress (ERS) and NLRP3 inflammasome activation. This study demonstrates Gen

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Area of Science:

Neuroscience
Pharmacology
Aging Research

Background:

Neuronal cell apoptosis and degeneration are hallmarks of natural aging.
Aging is associated with increased endoplasmic reticulum stress (ERS) and inflammasome activation.

Purpose of the Study:

To investigate the neuroprotective effects of genistein (Gen) on aged rat neurons.
To elucidate the underlying mechanisms involving ERS and NLRP3 inflammasome pathways.

Main Methods:

Fifty male Sprague-Dawley rats were divided into youth, aged, and genistein-treated groups.
Genistein was administered orally for 6 months to aged rats.
Western blotting was used to assess protein expression of key apoptotic and inflammatory markers.

Main Results:

Aged rats exhibited neuronal degeneration and increased expression of p-JNK, CHOP, NLRP3, Caspase-1, and ASC.
Genistein treatment improved hippocampal CA3 neuronal pathology and reduced apoptosis.
Genistein significantly decreased the expression of p-JNK, CHOP, NLRP3, Caspase-1, and ASC in aged rats.

Conclusions:

Genistein exhibits a protective effect on hippocampal neurons in aging rat brain.
Genistein inhibits the ERS apoptotic signaling pathway.
Genistein suppresses NLRP3 inflammasome activation in the aging brain.