Barbatic acid inhibits inflammatory responses and endothelial dysfunction in hypertension by regulating HIF1A/FLT1 pathway: A computer-aided biolabel research and experimental validation

Abstract

Hypertension is a prevalent cardiovascular and cerebrovascular condition encountered in clinical practice. It has emerged as a significant global public health challenge and is the leading risk factor for mortality. Barbatic acid has a pharmacological basis for preventing and treating hypertension, including mechanisms such as diuresis and anti-inflammatory effects. However, its therapeutic potential and mechanism of action remain incompletely understood. The purpose of this study is to investigate the therapeutic potential and mechanisms of action of barbatic acid in the treatment of hypertension. Based on the biolabel-led research model, bioinformatics was employed to conduct a comprehensive analysis of the therapeutic potential, advantages, and mechanisms of action of barbatic acid in treating hypertension. Ang II was utilized to establish a hypertensive cellular model, while L-NAME was employed to create an animal model of hypertension, thereby validating the findings from the biolabel analysis. Bioinformatics indicates that ten biolabels are implicated in the anti-hypertensive mechanism of barbatic acid. The primary targets are HIF1A and FLT1, which primarily contribute to inflammatory responses and endothelial dysfunction. Cell experiments demonstrate that barbatic acid can effectively enhance the proliferation ability of HUVECs and adjust the levels of ten biolabels and downstream targets. Animal experiments demonstrate that barbatic acid can effectively reduce blood pressure in hypertensive mice, significantly ameliorate associated pathological damage in the heart, kidney, and thoracic aorta tissues, and inhibit HIF1A/FLT1 levels in these mice, thereby improving the inflammatory response and endothelial dysfunction. The verification confirmed the analytical results of the biolabel research model. Barbatic acid has the capacity to inhibit the inflammatory response and endothelial dysfunction in hypertension by mediating the HIF1A/FLT1 pathway.