Jichu yixue yu linchuang (Feb 2021)
Myocardial inflammatory response in rats with vascular calcification caused by chronic kidney disease
Abstract
Objective To observe the myocardial inflammatory response and the expression of TLR4, IL-6 and TNF-α in rats with chronic kidney disease vascular calcification (CKD-VC). Methods Rats were divided into control group and CKD-VC group(adenine 200 mg/kg gavage+ high phosphorus 0.5 g/d drinking water). Blood routine and histological changes of heart, kidney and aorta were detected at 5 weeks. At 10 weeks, the serum of rats was collected to detect creatinine (Scr), urea nitrogen (BUN), serum calcium (Ca) and serum phosphorus (P); heart, kidney and aorta were taken, and histopathology change was observed by routine pathological examination; von Kossa staining to identify vascular calcification; Masson staining to detect renal fibrosis; immunohistochemistry to detect TLR4, IL-6 and TNF-α expression changes. Results As the CKD kidney disease progressed, the inflammatory lesions of the heart became more and more obvious. At 5th week, the counting of peripheral eosinophils and neutrophils in CKD-VC group was significantly higher than the control group (both P＜0.01), a small amount of lymphocytes infiltrated in one animal's myocardium; No vascular calcification was observed in the aorta by von Kossa staining. At 10th week, there were multiple myocardial necrosis in the heart with inflammatory cell infiltration, and TLR4, IL-6 and TNF-α were positive in the inflammation area; the incidence rate of vascular calcification identified by von Kossa staining in the CKD-VC group was 5/7. Conclusions Adenine gavage combined with the drinking water of high phosphate level induces CKD renal damage and vascular calcification, which simultaneously activates the expression of inflammatory factors such as TLR4, TNF-α and IL-6, causing chronic inflammatory damage of myocardium.
