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Published on: September 26, 2018
Colchicine attenuates diet-induced early aortic vascular remodeling in mice via modulation of inflammatory and cell
Amira I Shrief1, Sally Abdallah Mostafa2, Dina S Elshenawy3
1Department of Medical Histology and Cell Biology, Faculty of Medicine, Mansoura University, Mansoura 35511, Egypt; Medical Histology & Cell Biology Department, Faculty of Medicine, Horus University, New Damietta, Egypt.
Background:
Atherosclerosis (AS) contributes to cardiovascular diseases (CVDs) through inflammation and oxidative stress, with inflammation-associated cell death pathways as drivers of vascular injury.
Aim:
This study aimed to investigate the protective effects of colchicine on diet- induced vascular remodeling, focusing on caspase-1-dependent inflammatory signaling, caspase-3/gasdermin E (GSDME)-mediated cell death pathways, and toll-like receptor 4 (TLR4) signaling modulation.
Methodology:
Forty adult male C57BL/6 mice were categorized into four groups: control, colchicine-treated (0.25 mg/kg/day, i.p.), hypercholesterolemic, and hypercholesterolemic plus colchicine (0.25 mg/kg/day, i.p.). Mice were sacrificed after 12 weeks, and blood samples were collected. Thoracic aortic specimens were prepared for subsequent biochemical, molecular, histological, and ultrastructural analysis.
Results:
Colchicine administration significantly improved serum lipid profiles and modulated tissue oxidative stress by decreasing (1.8-fold) malondialdehyde (MDA) levels and increasing (1.75-fold) superoxide dismutase (SOD) levels. Colchicine significantly downregulated the mRNA expression levels of caspase-1 (2.4-fold), interleukin-1 beta (IL-1β) (3.6-fold), specificity protein 1 (SP1) (3.0-fold), signal transducer and activator of transcription 3 (STAT3) (2.4-fold), GSDME (3.3-fold), and TLR4 (2.6-fold) in the aortic samples, accompanied by near-normal immunohistochemical expression of caspase-3 and IL-1β. Furthermore, colchicine effectively preserved aortic wall structure, diminished fibrosis, and attenuated ultrastructural damage associated with inflammatory cell death.
Conclusion:
Colchicine displays protective effects against diet-induced vascular remodeling in mice, associated with the modulation of inflammatory and cell death pathway markers, alongside ultrastructural improvements. These findings support its therapeutic potential for mitigating vascular injury relevant to atherosclerosis, though further mechanistic validation is required.
