Yun Luan1, Sun Chao2, Zhi-Ye Ju3, Jue Wang2, Xia Xue4, Tong-Gang Qi2, Guang-Hui Cheng2, Feng Kong5. 1. Central Research Laboratory, The Second Hospital of Shandong University, Jinan, China. Electronic address: Y_luan@aiyun.com. 2. Central Research Laboratory, The Second Hospital of Shandong University, Jinan, China. 3. Department of Radiology, Rizhao City People's Hospital, Rizhao, Shandong 276807, China. 4. Department of Pharmacy, The Second Hospital of Shandong University, Jinan, China. 5. Central Research Laboratory, The Second Hospital of Shandong University, Jinan, China. Electronic address: fengk1970@163.com.
Abstract
BACKGROUND: Baicalin has been shown to possess various pharmacological actions, a recent study revealed that baicalin can attenuate pulmonary hypertension and pulmonary vascular remodeling through the inhibition of pulmonary artery smooth muscle cell proliferation, however, the potential mechanism remains unexplored. In this study, we investigated the therapeutic effect of baicalin on a rat model of monocrotaline (MCT)-induced pulmonary arterial hypertension (PAH) and attempted to further clarify the possible mechanisms underlying the anti-inflammatory. METHODS AND RESULTS: Our research showed that compared with MCT-induced PAH model rats, rats administered intragrastically with 100mg/kg baicalin showed the following after two weeks: the right ventricular systolic pressure (RVSP) and the right ventricle/left ventricle plus septum (RV/LV+S) ratio were lower (P<0.05); the intima thickening and luminal stenosis were improved (P<0.05); the mRNA levels of tumor necrosis factor alpha (TNF-α), interleukin-11β (IL-1β), IL-6, and endothelin-1 (ET-1) were obviously reduced by quantitative reverse transcription-polymerase chain reaction (qRT-PCR); the protein expression of transforming growth factor-β1 (TGF-β1), intercellular cell adhesion molecule-1 (ICAM-1) and nuclear factor-κB (NF-κB) were significantly decreased (P<0.05); and the expression of inhibitor of NF-κB (I-κB) was increased (P<0.05) through immunohistochemical and western blot. CONCLUSION: We studied the protective effects of baicalin against the lung and heart damage in experimental PAH rats; the therapeutic effects maybe through inhibiting vascular endothelial inflammatory response.
BACKGROUND:Baicalin has been shown to possess various pharmacological actions, a recent study revealed that baicalin can attenuate pulmonary hypertension and pulmonary vascular remodeling through the inhibition of pulmonary artery smooth muscle cell proliferation, however, the potential mechanism remains unexplored. In this study, we investigated the therapeutic effect of baicalin on a rat model of monocrotaline (MCT)-induced pulmonary arterial hypertension (PAH) and attempted to further clarify the possible mechanisms underlying the anti-inflammatory. METHODS AND RESULTS: Our research showed that compared with MCT-induced PAH model rats, rats administered intragrastically with 100mg/kg baicalin showed the following after two weeks: the right ventricular systolic pressure (RVSP) and the right ventricle/left ventricle plus septum (RV/LV+S) ratio were lower (P<0.05); the intima thickening and luminal stenosis were improved (P<0.05); the mRNA levels of tumor necrosis factor alpha (TNF-α), interleukin-11β (IL-1β), IL-6, and endothelin-1 (ET-1) were obviously reduced by quantitative reverse transcription-polymerase chain reaction (qRT-PCR); the protein expression of transforming growth factor-β1 (TGF-β1), intercellular cell adhesion molecule-1 (ICAM-1) and nuclear factor-κB (NF-κB) were significantly decreased (P<0.05); and the expression of inhibitor of NF-κB (I-κB) was increased (P<0.05) through immunohistochemical and western blot. CONCLUSION: We studied the protective effects of baicalin against the lung and heart damage in experimental PAH rats; the therapeutic effects maybe through inhibiting vascular endothelial inflammatory response.