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To explore the protective effect of CGRP on arterial injury.
Rat VSMC was induced by angiotensin II (Ang II) and divided into three groups. The experimental group received CGRP treatment, the control was injured without intervention, and the blank group was conventional cultured VSMC. VSMC phenotype marker α-SMA and osteopontin (OPN), and ERK1/2 phosphorylation were tested by Western blot. Cell cycle, apoptosis, and proliferation were analyzed by flow cytometry.
α-SMA expression significantly elevated, while OPN level obviously reduced in VSMC after CGRP intervention (P < 0.05). Cell percentage in S phase and proliferation index in experimental group markedly declined compared with control after 6 h, 12 h, and 24 h (P < 0.05). Cell percentage in S phase and apoptosis index gradually decreased in experimental group following CGRP intervention time extension (P < 0.05). ERK1/2 and p-ERK1/2 proteins in experimental group were obviously lower than that in control (P < 0.05) and declined following treatment time elongation (P < 0.05).
CGRP may regulate VSMCs phenotype and restrain cell proliferation via inhibiting ERK1/2 signaling pathway activation.