Assessment of indicators of myocardial fibrosis in experimental type 2 diabetes mellitus and with administration of L-arginine and N-acetyl-L-cysteine
DOI:
https://doi.org/10.26641/1997-9665.2026.2.27-34Keywords:
type 2 diabetes mellitus, cardiomyopathy, myocardial fibrosis, collagen type 1, L-arginine, N-acetyl-L-cysteine, morphometry, ratsAbstract
Background. The study is devoted to diffuse myocardial fibrosis in type 2 diabetes mellitus and the possibilities of its correction with the help of L-arginine and N-acetylcysteine. The work evaluates the potential of these compounds to modify already formed structural changes in the heart and the possibility of preventing further damage in conditions of insulin resistance and metabolic overload. Aim. To evaluate the morphological effects of L-arginine and N-acetyl-L-cysteine on interstitial and perivascular components of myocardial fibrosis in experimental type 2 diabetes mellitus (T2DM) in Wistar rats. Methods and Results. The study was conducted on 42 Wistar rats (18-20 months old). T2DM was induced by a high-fat diet combined with streptozotocin (30 mg/kg). The animals were divided into groups: control, T2DM without correction, T2DM treated with L-arginine (1.5 g/kg), and T2DM treated with N-acetyl-L-cysteine (1.5 g/kg) for 2 weeks. Masson's trichrome staining and immunofluorescence analysis for collagen type 1 were performed. T2DM was found to increase interstitial fibrosis by 3.94 times and perivascular fibrosis by 2.24 times compared to the control group. The content of collagen type 1 increased by 492 %. L-arginine administration led to a further increase in interstitial fibrosis (1.21 times) and collagen type 1 content (by 18 %). N-acetyl-L-cysteine treatment promoted a 0.74-fold reduction in interstitial fibrosis but was accompanied by a 44 % increase in collagen type 1 expression. Conclusions. Experimental T2DM forms pronounced diffuse myocardial fibrosis dominated by the interstitial component and collagen type 1 accumulation. L-arginine does not exhibit a fibroprotective effect in this model. N-acetyl-L-cysteine partially reduces interstitial fibrosis but does not prevent the pathological expression of collagen type 1.
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