Reduces depression symptoms brought on by long-term stress with Sanggenon C

Abstract

The goal of this study is to determine if Sanggenon C alleviates depression in Wistar rats subjected to chronic
unexpected mild stress (CUMS).
Methods: A forced swimming test and a sucrose preference experiment were used to evaluate Sanggenon C's anti-
depressant impact. Histological investigations were conducted on the cortex and hippocampus using hematoxylin
and eosin (H & E) stains, while an open-field test was used to quantify the locomotor change produced by CUMS.
To assess cell death, researchers used TUNEL staining, which stands for terminal deoxynucleotidyl transferase
dUTP nick end labeling. We also used Western blotting to assess the levels of AMP-activated protein kinase
(AMPK) phosphorylation and the expressions of brain-derived neurotrophic factor (BDNF), Bax, Bcl-2, cleaved
caspase-3, LC3, Beclin, and P62.
Sanggenon C had a substantial impact on open-field CUMS rats, increasing their preference for sucrose,
decreasing their immobility time in the forced swimming test, and increasing the size of the crossing squares and
rearing periods (p < 0.05).
Nuclear shrinkage and damage in the cortex and hippocampus were both alleviated by sanggenon C. Additionally,
Sanggenon C controlled the expression of autophagy-associated molecules (LC3, Beclin, and p62), proteins linked
with apoptosis (Bax, Bcl-2, and cleaved caspase-3), and other proteins. There was an increase in BDNF expression
and AMPK phosphorylation that Sanggenon C showed.
Results: Sanggenon C activates the AMPK pathway in CUMS rats, which enhances neuroprotection and depressed
behavior while inhibiting apoptosis and inducing neuronal autophagy. To completely comprehend the therapeutic
importance of Sanggenon C-mediated AMPK activation in various cellular settings as prospective therapeutic
targets, more study is necessary.