AI Article Synopsis
- The study explores how ligustilide (LIG) affects cell death in cerebellar granule neurons caused by low potassium levels.
- LIG demonstrated protective effects against low potassium-induced apoptosis, showing that higher concentrations led to increased survival rates and activation of key signaling proteins.
- The protective action of LIG involves GABA receptor activation and the insulin-like growth factor 1 (IGF-1) signaling pathway.
Article Abstract
Objective: To investigate the effect of ligustilide (LIG) on low potassium-induced apoptosis in primary cultured cerebellar granule neurons (CGN).
Methods: Apoptosis was induced by low potassium in cultured neonatal rat CGN in vitro. The CGN was divided into control/model/CGP54626 + LIG and LIG group. The neuronal viability of each group was measured by MTT assay. The protein expression levels of the key insulin-like growth factor 1 (IGF)-1 signaling effectors,including the phosphorylated IGF-1 receptor (IGF-1R), Akt, ERK1/2, CREB and activated caspase 3 were examined by Western blot analysis.
Results: LIG ranging from 2.5 to 20 micromol/L could protect against low potassium-induced apoptosis of CGN ini a concentration-dependent manner. 20 micromol/L LIG significantly induced upregulation of the phosphorylated levels of IGF-1, Akt, ERK1/2 and CREB, and downregulation of cleaved-caspase 3 expression, which could be blocked by a selective gamma-aminobutyric acid B (GABAs) receptor antagonist CGP54626.
Conclusion: LIG concentration-dependently protects against low potassium-induced apoptosis in CGN at least partly through GABAa receptor activation and its downstream IGF-1 signaling pathway.
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