Effect of Rhodomyrtus tomentosa (Aiton) Hassk. on aortic hyperglycemia via JAK family expression

Context: Hyperglycemia is a significant contributor to the development of atherosclerosis and is a major risk factor. The process initiates with the phosphorylation of JAK1 and JAK2, subsequently leading to the activation of STAT3, which results in atherosclerotic damage to vascular endothelial cells. Rhodomyrtus tomentosa is an antioxidant botanical in traditional medicine with the capacity to mitigate oxidative stress. Aims: To analyze JAK family expression in aorta tissue after administration of R. tomentosa. Methods: A Completely Randomized Design (CRD) was utilized to test Wistar rats in six groups: K+: alloxan-induced diabetes, K-: untreated animals, and K0: diabetic rats + metformin. Groups K1, K2, and K3 received R. tomentosa at 100, 150, and 200 mg/kg BW. R. tomentosa was taken orally for two weeks. Next, the animals were dissected to take the aorta for analysis of immunohistochemistry with JAK family expression and also for analysis of the lumen and thickness of the aorta. Results: Hyperglycemic aortic tissue alters histologically, changing lumen size and tunica intima thickness and also media tunica layers. Foam cells produce fat and plaque streaks that thicken and restrict blood channel lumens. This restriction can slow blood flow. R. tomentosa restored lumen size similar to the untreated group. JAK1 and JAK2 inhibit pro-inflammatory protein function; however, JAK3 expression in aortic tissue decreases when R. tomentosa dosage increases. Conclusions: Hyperglycemic aortic tissue has histological modifications, such as changes in lumen diameter and hypertrophy of the tunica intima and media, resulting in foam cell development, lipid streaks, and plaque-induced vascular constriction. Administering R. tomentosa restores lumen size and modulates JAK protein expression, with JAK1 and JAK2 levels inhibiting pro-inflammatory proteins, while JAK3 expression diminishes with increasing dosage.