ABSTRACT
Objective To examine the role of connective tissue growth factor (CTGF) in a rat model of paraquat (PQ)-induced pulmonary fibrosis. Methods In the laboratory of Medical School of Nanjing University, 48 adult male Sprague-Dawley (SD) rats were randomly(random number) divided into two groups. The experimental group received a single intraperitoneal injection of PQ (30 mg/kg), while the control group received an equivalent volume of sterile saline. The rats were then sacrificed and the left lungs were collected on 7th, 14th and 28th day, respectively. HE staining, Masson staining and hydroxyproline content analysis were used to determine the quantity of collagen, and the fibrosis process and severity were evaluated. Western blotting and immunohistochemical staining was used to detect the expression of CTGF. MRC-5 human lung fibroblasts were exposed to different concentrations of PQ (50-500 μmol/L) for 3 days. The proliferation, migration and differentiation of MRC-5 cells were investigated by CCK8, Transwell and Western blotting after exposing with various concentrations of CTGF (50-200 ng/mL). Data was analyzed with SPSS18.0. Results At 2 weeks after PQ administration, lung tissue sections exhibited a marked thickening of the alveolar walls with an accumulation of interstitial cells witha fibroblastic appearance. Masson staining revealed a patchy distribution of collagen deposition, indicating pulmonary fibrogenesis. Western-blott and immunohistochemical staining demonstrated that CTGF expression was significantly upregulated in the PQ-treated group (P<0.01). Similarly, CTGF expression in PQ-treated MRC-5 cells was increased in a dose-dependent manner (P<0.01). In addition, CTGF promoted the proliferation and migration of MRC-5 cells (P<0.01), and induced the differentiation of fibroblasts into myofibroblasts. Conclusions These findings demonstrate that PQ can increase CTGF expression, which may be important in PQ-induced pulmonary fibrogenesis. Therefore, this growth factor can be considered as a potential pharmacological target.
ABSTRACT
Gastroesophageal reflux disease(GERD) is a common upper gastrointestinal tract dysfunctional disease in paediatrics, which has specifical clinical manifestations due to reflux. GERD can be diagnosed by clinical symptoms associated with related examinations.The treatment of GERD involves general treatment,medication, surgery. Proton pump inhibitor is the most frequently used drug.
ABSTRACT
Objective To investigate the curative effect of sodium nitroprusside in the treatment of EV71-related pneumoedema/pneumorrhagia and hypotension in this study. Methods This was a retrospective study of a total 10 children with EV71-related pneumoedema/pneumorrhagia treated with sodium nitroprusside using case-control methods. The clinical manifestations and outcomes of the 10 children (present cohort) were compared with those of 8 children (past cohort) who had EV71-related pneumoedema/pneumorrhagia without sodium nitroprusside. Results Among these 10 patients,all were at the appearance of pneumoedema/pneumorrhagia, cardiac arrhythmia and hypotension. Two patients showed severe cardiac arrhythmia, two patients showed cardiac arrest for many times. All 10 patients were treated with mechanical ventilation and other conventional treatments. At the first time of the manifest of hypotension,sodium nitroprusside were put into practice in all 10 patients. Ten patients were treated with intravenously sodium nitroprusside in the stage of hypotension by maxi30 min ～ 1 h,the patients showed an improvement in vultus,pulse and peripheral circulation and decrease of heart rate and elevation of blood pressure after 30 min ～2 h,but at least 2～6 h later,the blood pressure tended to stabilize at normal standard. Conclusion Hypotension is the intensive stage in EV71-related hand,foot and mouth disease ,and the shock syndrome caused by acute left ventricular disorder is related to sympathetic nerve activity. Sodium nitroprusside can effectively reduce the cardiac afterload,and correct shock and improve the prognosis.