Our data showed selleck chemical that after treated with DCQD, the production of NO in pancreatic tissues was increased, accompanying the increase of apoptosis with the decrease of inflammatory cells infiltration and pathological scores in pancreatic tissues. This indicated that the increase of NO and iNOS was not the reason of pancreatic tissue damage, but a protective factor might be involved in inducing apoptosis and reduce pancreatic tissue pathological severity. ROS and nitrogen oxide species play important and different roles in various physiological and pathological states. In our study, DCQD exerting an opposite regulation on NO and ROS may come from its scavenging effects which remain to be understood.

These findings provided evidence that treated with DCQD reduce the generation of ROS and increase the NO pancreatitis acinar cells, therefore regulate apoptosis/necrosis switch, induce apoptosis of injured acinar cells and inhibit the subsequent amplifying inflammatory response, which in turn protects against AP. In the present study, we introduce the ideas and methods of translating research into traditional Chinese medicine, and this is the first time to research the way of compound Chinese herb formula DCQD regulating apoptosis/necrosis switch on AP in vitro and in vivo. Here we conclude that DCQD could inhibit the local and systematic inflammatory response and alleviate the pancreatic damage via regulating the pancreatic cell necrosis/apoptosis switch. Future study should be directed at signaling pathways of ROS and NO in regulating injured pancreatitis acinar cell apoptosis by the treatment of DCQD.

Footnotes Competing Interests: The authors have declared that no competing interests exist. Funding: The study was supported by the grants of Natural Science Foundation of China (No: 30400576, 30973711 and 30672588). The funder had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
Preterm prelabor rupture of membranes (PPROM) occurs in one third of all preterm deliveries and represents a specific subset of spontaneous preterm deliveries. It is defined as spontaneous rupture of the membranes with the leakage of amniotic fluid at least two hours before the onset of regular uterine activity in the gestational age below 37 weeks [1].

Several areas of controversy in the management of PPROM pregnancies exist, but at least three of the most important strategies are widely accepted by the broad obstetrician community: i) the use of antibiotics to prolong the AV-951 time period between rupture of the membranes and delivery, ii) the administration of corticosteroids below gestational age of 32 weeks to diminish the risk of respiratory disease in newborns, and iii) the application of magnesium sulfate for fetal neuroprotection [2]�C[8]. Subsequently, either expectant or active management must be chosen.