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.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117 FEBS+Open+Bio
2017 ; 7
(4
): 477-484
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Activation of PPAR? by baicalin attenuates pulmonary hypertension in an infant
rat model by suppressing HMGB1/RAGE signaling
#MMPMID28396833
Chen Z
; Wang Q
FEBS Open Bio
2017[Apr]; 7
(4
): 477-484
PMID28396833
show ga
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.
ELISAs were used to determine concentrations of high-mobility group box 1
(HMGB1), secretory receptor for advanced glycation end products (sRAGE),
interleukin 6 (IL6) and transforming growth factor ? (TGF?1) in bronchoalveolar
lavage fluid (BALF). Electrophoretic mobility shift and phosphorylation in
nuclear extracts were used to evaluate the activation of peroxisome
proliferator-activated receptor ? (PPAR?). Western blotting was used to detect
the expression levels of heme oxygenase 1 (HO1), HMGB1, RAGE, IL6 and TGF?1 in
lung tissue. Baicalin administration significantly attenuated mPAP, RVEDP and RV
hypertrophy in infant rats with PH. HMGB1, sRAGE, IL6 and TGF?1 levels in BALF
were also reduced by baicalin treatment. Baicalin activated PPAR?, which promoted
expression of HO1. Furthermore, expression levels of HMGB1, RAGE, IL6 and TGF?1
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? that inhibited HMGB1/RAGE inflammatory signaling was involved.