Effects Of Cinnamaldehyde On Proliferation And Collagen Synthesis Of Rats Cardiac Fibroblasts Induced By High Glucose And Its Mechanisms

Objective：In diabetic cardiomyopathy(DCM)，myocardial fibrosis and collagen depositionare the primary structural changes.Hyperglycemia plays a central role in thepathogenesis of DCM and triggers a series of maladaptivestimuli that result inmyocardial fibrosis and collagen deposition. In vitro,high glucose can promote CFsproliferation and collagen synthesis. Some studies have shown that the ERK1/2cascade is a potent regulatory pathway in CFs proliferation and collagen types I andIII expression by high glucose,which suggests that the ERK1/2plays an essentialrole in the control of collagen deposition by high glucose.Cinnamaldehyde(Cin) is a principle and a bioactive compound isolated from theleaves of Cinnamomum osmophloeum kaneh. Studies have demonstrated thatcinnamaldehyde has immunomodulatory, anti-tumourigenic effects, and anti-diabeticeffects etl.Cinnamaldehyde is widely used to treat diabetes in traditional system ofmedicine. A study demonstrated that cinnamaldehyde impaired high glucose-inducedproliferation and hypertrophy in renal interstitial fibroblasts that may be dependent oninactivation of the ERK pathway.The order of this study is to explore the effects of Cin on proliferation andcollagen typesⅠ and Ⅲsynthesis of cardiac fibroblasts(CFs) induced by highglucose(HG) in diabetic cardiomyopathy (DCM),and the potential mechanism.Methods：CFs was isolated from1-3-day-old SD rats and cultured in DMEM with10%fetal bovine serum(FBS), CFs proliferation was determined by MTT. The expressionof collagen typesⅠ and Ⅲ was detected by ELISA.The mRNA expression of collagentypesⅠ and Ⅲ was determined by RT-PCR. The expression of ERK1/2andphosphor-ERK1/2(pERK1/2) protein was detected by Western-blot.Results:Compared with the control group, the proliferation,collagen types Ⅰ andⅢprotein and mRNA expression of of CFs in high glucose group were higher (P <0.05).Compared with the high glucose group,Cin down-regulated proliferation andthe mRNA expression of collagen types Ⅰa ndⅢ in a dose-and time-depedentmanner and it decreased the protein expression of p-ERK1/2was lower (P <0.05).Conclusion:Cinnamaldehyde inhibited the proliferation and collagen types Ⅰ andⅢsynthesis of CFs induced by high glucose,and the mechanism may be related withinhibiting the activity of ERK1/2signaling pathway.