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हमारा समूह 1000 से अधिक वैज्ञानिक सोसायटी के सहयोग से हर साल संयुक्त राज्य अमेरिका, यूरोप और एशिया में 3000+ वैश्विक सम्मेलन श्रृंखला कार्यक्रम आयोजित करता है और 700+ ओपन एक्सेस जर्नल प्रकाशित करता है जिसमें 50000 से अधिक प्रतिष्ठित व्यक्तित्व, प्रतिष्ठित वैज्ञानिक संपादकीय बोर्ड के सदस्यों के रूप में शामिल होते हैं।

ओपन एक्सेस जर्नल्स को अधिक पाठक और उद्धरण मिल रहे हैं
700 जर्नल और 15,000,000 पाठक प्रत्येक जर्नल को 25,000+ पाठक मिल रहे हैं

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अमूर्त

Panax Notoginsenosides Attenuates Pleural Inflammation in Rabbit Model

Helin Zhang, Ruilin Liu, Hongle Yang, Zhichao Wang and Chenli Li

to investigate the effect of intrapleural PNS on rabbit pleural inflammation reaction, and determine the levels of transforming growth factor β1 (TGF-β1) and Vascular Endothelial Growth Factor (VEGF). Forty New Zealand white rabbits were divided into four groups. The rabbit pleural inflammation reaction model was established by injection of tetracycline hydrochloride solution into pleural cavity. Then PNS, urokinase (UK) and PBS were injected into the pleural cavity as experiment groups. While tetracycline hydrochloride solution was replaced by phosphate buffer solution (PBS) as control group. The pleural effusion was collected at 24 h, 48 h, 72 h and 96 h in all groups, and then biochemical indicators, TGF-β1 and VEGF were detected. On day 14, all animals were killed and pleural tissues were collected to perform hematoxylin eosin (HE) and Masson trichrome staining. The results indicated that levels of TGF-β1 and VEGF were significantly lower in PNS group than that in UK group and PBS group (P<0.05); and the levels of VEGF were maximum at 48 h in three experimental groups. The thickness of pleural was thinner in PNS group, and the number of inflammatory cells and fibroblasts was also decreased in PNS group. In conclusion, PNS could reduce production of TGF-β1 and VEGF, reduce number of inflammatory cells and fibroblast, and inhibit collagen production, which had better effects compared with UK. Our findings provide a new treatment strategy for inflammation reaction.