HMGB1 review: HMGB1-RAGE signaling research

This is a study to investigate the efficacy of baicalin in infant rodent models and to further explore its underlying mechanisms. Pulmonary hypertension (PH) is a vascular disease, its inflammatory factors are closely related to its pathogenesis, leading to right ventricular hypertrophy and heart failure. Baicalin has a strong anti-in activity. The rat model of infants and young children was induced by hypoxia, and the rats were treated with baicalin in an incremental dose. The mean pulmonary arterial pressure (mPAP) and RV end diastolic pressure (RVEDP) were measured using invasive hemodynamic methods. RV hypertrophy was assessed by large-scale pathology and histology. The use of ELISA to determine the secretion of high mobility group 1 (HMGB1), advanced glycation end products (sRAGE), interleukin 6 (IL6) and transforming growth factor b (TGFb1) in bronchoalveolar lavage fluid (BALF) Body concentration. The activation of the peroxisome proliferator-activated receptor c (PPARc) was assessed using electrophoretic mobility and phosphorylation in the nuclear extract. The expression levels of heme oxygenase 1 (HO1), HMGB1, RAGE, IL6 and TGFb1 in lung tissue were detected by Western blotting. Effects of baicalin on mPAP, RVEDP and RV hypertrophy in infants and young children. The levels of HMGB1, sRAGE, IL6 and TGFb1 in BALF were also decreased by baicalin treatment. Effect of baicalin on PPARc and promotion of HO1 expression. In addition, the expression levels of HMGB1, RAGE, IL6 and TGFb1 in lung tissue were significantly decreased in a dose-dependent manner. The efficacy of baicalin in infants with PH. Involving activation of PPARc that inhibits HMGB1 / RAGE activation signaling.

In conclusion, studies have shown that PPARc signaling inactivation is one of the mechanisms of PH. Thus, as a downstream medium of PPARc, HO1 expression is downregulated. As a result, the HMGB1-RAGE axis was activated to induce airway and pulmonary vascular remodeling. Baicalin acts as an activator of PPARc, which reduces the pH of the infant rat. This therapeutic effect is associated with HO1 induction and HMGB1-RAGE axis inhibition. As can be seen from this study, activation of PPARc will be an effective strategy for the treatment of PH. In addition, compounds containing baicalin and baicalin may have therapeutic value in PH.

Key conception:

PULMONARY hypertension

INFANT diseases

HIGH mobility group proteins

CELL interaction (Biology)

ANTI-inflammatory agents

RATS as laboratory animals


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