ABSTRACT Purpose: Our previous study showed that Er-Bai-Tang decoction (EBT) could effectively improve Parkinson’s disease (PD) patients’ quality of life, sleep, mood, and cognitive disorders, but the mechanism of EBT to treat PD was unclear. So, our study aimed to explore the mechanism of EBT to treat PD via p38 mitogen-activated protein kinases (MAPK) pathway and intestinal flora. Methods: In our study, the PD rat model was established by subcutaneously injecting 2 mg/kg/d rotenone solution, and 23.43 g/kgEBT was used to treat PD model rats. Results: Behavioral test showed that EBT could reverse the motor impairment in the PD model rats. Hematoxylin and eosin result showed that EBT could reduce the cell necrosis in the SNpc area of the PD model rats. Western blotting and real time-polymerase chain reaction showed that EBT could decrease the p38 MAPK expression in the SNpc area of the PD model rats. 16s rRNA sequencing analysis showed that EBT could improve the composition of intestinal flora in the PD model rats. Rikenellaceae at family level and Alistipes and Allobaculum at the genus level were the key species in the PD development and EBT treatment to PD. KEGG showed that EBT might change the iron uptake in PD rats. Conclusions: EBT could improve the motor symptoms and neuronal injury in the PD model rat, and its mechanism may be related to decreasing p38 MAPK pathway and improving the composition of intestinal flora. Purpose ErBaiTang Er Bai Tang (EBT Parkinsons Parkinson s (PD patients life sleep mood disorders unclear So p p3 mitogenactivated mitogen activated (MAPK Methods mgkgd mg kg d solution 2343 23 43 23.4 gkgEBT g kgEBT rats Results timepolymerase time polymerase Conclusions 234 4 23.

Abstract Objective The paper studied the effects of Rhynchophylline on the leptin-mediated JAK2/STAT3 pathway in hypothalamus. Using the leptin / leptin receptor and leptin-mediated JAK2/STAT3 pathway as an entry point, the research evaluated the effect of the hypotensive drug, and clarified the preliminary mechanism, expecting to provide new therapeutic ideas for essentially improving obese hypertension, balancing the body's neuro-endocrine function, and preventing the occurrence of cardiovascular diseases. Methods: A model of obese hypertensive rats was established, and the serum lipids, Lep, AngII, NPY and NO contents in each group of rats were measured. Immunohistochemical staining was used to observe the distribution of leptin receptor (LepR) and angiotensin II type 1 receptor (AT1R) in hypothalamus and aorta of rats. Western Blot method was employed to detect JAK2, STAT3, SOCS3, LepR and AT1R protein expressions in the hypothalamus of rats. After the third ventricle injection of AG490, Western blot was applied to detect the expressions of various proteins. Results: Rhynchophylline can significantly reduce AngII, Lep, and NPY levels in serum circulation. Immunohistochemistry showed that the hypothalamus and aorta AT1R distribution was significantly reduced, the hypothalamic LepR distribution increased, and the aortic LepR distribution decreased. The expressions of JAK2, LepR, and STAT3 proteins in the hypothalamus increased significantly, and the expressions of SOCS3 and AT1R proteins significantly decreased. After injection of AG490 in the third ventricle of Rhynchophylline rats, the expressions of JAK2 and STAT3 in the hypothalamus decreased significantly, while the SOCS3expression increased remarkably. Conclusion: Rhynchophylline can reduce blood lipid, as well as serum AngII, Lep, and NPY levels, increase serum NO levels in obese hypertension rats. Rhynchophylline can effectively inhibit the expression of SOCS3 by activating the JAK2/STAT3 pathway in the hypothalamus. Therefore, it is speculated that the JAK2/STAT3 signaling pathway is the main pathway through which Rhynchophylline plays a role in improving selective leptin resistance and reducing blood pressure and weight.

Abstract A 32-month-old girl with patent ductus arteriosus, false tendon of left ventricle, mild pulmonary hypertension, and chronic cardiac insufficiency (cardiac function level I-II) was misdiagnosed with Marfan Syndrome and there was no improvement in her physical growth after operation for this disease. The preterm baby was finally diagnosed with Myhre Syndrome by clinical phenotypes and mutation of SMAD4 gene. 32monthold monthold 32 month old arteriosus ventricle hypertension III I II I-II disease SMAD gene 3