Activation of PPAR γ by baicalin attenuates pulmonary hypertension in an infant rat model by suppressing HMGB 1/ RAGE signaling

Pulmonary hypertension ( PH ) is a vascular disease, and proinflammatory factors are strongly implicated in its pathogenesis, causing right ventricular ( RV ) hypertrophy and heart failure. Baicalin exhibits potent anti‐inflammation activity. This study aimed to investigate the curative effects of baicalin in an infant rodent model of PH and to further explore the underlying mechanisms. A PH model in infant rats was induced by hypoxia and the resulting rats were administered baicalin in incremental dosages. Invasive hemodynamic methods were used to measure mean pulmonary arterial pressure ( mPAP ) and RV end‐diastolic pressure ( RVEDP ). RV hypertrophy was assessed by mass pathology and histology. ELISA s were used to determine concentrations of high‐mobility group box 1 ( HMGB 1), secretory receptor for advanced glycation end products ( sRAGE ), interleukin 6 ( IL 6) and transforming growth factor β (TGFβ1) in bronchoalveolar lavage fluid ( BALF ). Electrophoretic mobility shift and phosphorylation in nuclear extracts were used to evaluate the activation of peroxisome proliferator‐activated receptor γ ( PPAR γ). Western blotting was used to detect the expression levels of heme oxygenase 1 ( HO 1), HMGB 1, RAGE , IL 6 and TGFβ1 in lung tissue. Baicalin administration significantly attenuated mPAP , RVEDP and RV hypertrophy in infant rats with PH . HMGB 1, sRAGE , IL 6 and TGFβ1 levels in BALF were also reduced by baicalin treatment. Baicalin activated PPAR γ, which promoted expression of HO 1. Furthermore, expression levels of HMGB 1, RAGE , IL 6 and TGFβ1 in lung tissue were dramatically decreased by baicalin in a dosage‐dependent manner. Baicalin showed curative effects in infant rats with PH . Activation of PPAR γ that inhibited HMGB 1/ RAGE inflammatory signaling was involved.