Objective To determine the effect of prokinetic agents such as domperidone, mo-sapride, clarithromycin, and itopride on the electrical activity of the stomach and duodenum in SD rats, and also to explore the mechanism. Methods The organism functional experiment system BL-420E was used to record the myoelectrical activity in the stomach and duodenum of SD rats in all groups using domperidone, mosapride, itopride, clarithromycin, and physiological saline on the inter-digestive phase. The effect of the prokinetic agents on the amplitude and freqency of gastric and duo-denal electromyologram in the SD rats was compared. The antagonists such as atropine, phento-lamine, and propranolol were added to investigate the mechanism of action with all prokinetic agents. Results All prokinetic agents increased the amplitude and frequency of gastric and duodenal fast waves in the SD rats (P<0.05). The effect of itopride was the most obvious among the 3 groups (P<0.05), and clarithromycin had the weakest effect (P<0.05). The amplitude and frequency of gastric and duodenal fast waves in the SD rats in the groups of clarithromycin, domperidone, mosa-pride, itopride, and physiological saline were inhibited by atropine (P<0.05) , but not by phento-lamine and propranolol. Conclusion Itopride, mosapride, domperidone, and clarithromycin can in-crease the amplitude and frequency of gastric and duodenal fast waves in the SD rats. The mechanism may be related to cholinergic receptors, but not adrenergic receptors.

Objective To investigate the inhibition of Eriobotryae Folium from twenty different districts towards phosphodiesterase 4(PDF4) in vitro.Methods The Eriobotryae Folium were extracted with 95％ ethanol reflux and the inhibition rates against PDE4D2 were carried out by liquid scintillation counting method.Results All the samples exhibited inhibitory activities towards PDE4 at 5 mg/L.Among them,nine samples were of the inhibition rate less than 80％,eleven samples were of more than 80％ inhibition and eight samples were of more than 90％ inhibition.Conclusion The Eriobotryae Folium shows significantly different inhibitory activities towards PED4.

Renal interstitial fibrosis (RIF) is the crucial pathway in chronic kidney disease (CKD) leading to the end-stage renal failure. However, the underlying mechanism of Shen Qi Wan (SQW) on RIF is not fully understood. In the current study, we investigated the role of Aquaporin 1 (AQP1) in SQW on tubular epithelial-to-mesenchymal transition (EMT). A RIF mouse model induced by adenine and a TGF-β1-stimulated HK-2 cell model were etablished to explore the involvement of AQP 1 in the protective effect of SQW on EMT in vitro and in vivo. Subsequently, the molecular mechanism of SQW on EMT was explored in HK-2 cells with AQP1 knockdown. The results indicated that SQW alleviated kidney injury and renal collagen deposition in the kidneys of mice induced by adenine, increased the protein expression of E-cadherin and AQP1 expression, and decreased the expression of vimentin and α-smooth muscle actin (α-SMA). Similarly, treatmement with SQW-containing serum significantly halted EMT process in TGF-β1 stimulated HK-2 cells. The expression of snail and slug was significantly upregulated in HK-2 cells after knockdown of AQP1. AQP1 knockdown also increased the mRNA expression of vimentin and α-SMA, and decreased the expression of E-cadherin. The protein expression of vimentin increased, while the expression of E-cadherin and CK-18 significantly decreased after AQP1 knockdown in HK-2 cells. These results revealed that AQP1 knockdown promoted EMT. Furthermore, AQP1 knockdown abolished the protective effect of SQW-containing serum on EMT in HK-2 cells. In sum, SQW attentuates EMT process in RIF through upregulation of the expression of AQP1.
Drugs, Chinese Herbal/pharmacology* ; Humans ; Animals ; Mice ; Male ; Cell Line ; Rats ; Kidney/physiology* ; Fibrosis/drug therapy* ; Renal Insufficiency, Chronic/drug therapy* ; Adenine ; Epithelial-Mesenchymal Transition ; Aquaporin 1/metabolism*