ABSTRACT
Acute pancreatitis (AP) is an inflammatory disorder of pancreas and common digestive diseases, effective drug for AP is few. As an analog of active center of Reg3α, the biological activities of HTD4010 are similar to Reg3α. This study aimed to explore whether HTD4010 could decrease the inflammatory response and pancreatic injury in hypertriglyceridemic-AP (HTG-AP), and explore underlying mechanisms. This study was shown that the administration of HTD4010 could decrease the inflammatory response, reduce acinar cell injury (both apoptosis and necroptosis) and damage of lung tissue in HTG-AP. Moreover, HTD4010 down-regulated the expression of TLR4 and NF-κB protein. These results showed that HTD4010 could alleviate the severity of AP possibly by TLR4/NF-κB signaling pathway in HTG-AP.
Subject(s)
NF-kappa B , Pancreatitis , Acute Disease , Animals , Disease Models, Animal , Mice , NF-kappa B/metabolism , Pancreas/metabolism , Pancreatitis/drug therapy , Pancreatitis/metabolism , Peptides/metabolism , Toll-Like Receptor 4/metabolismABSTRACT
Mutations in the precore and core promoter regions of hepatitis B 'e' antigen (HBeAg) are implicated in HBeAgnegative chronic hepatitis B virus (HBV) infection (CHB). The objective of the current study was to investigate novel mutant patterns that lead to HBeAgnegative CHB. The . PreX-X genomic region from the sera of HBVinfected patients was amplified, and analysis of the sequences displayed a unique deletion region, 234 nucleotides in length, which was observed in 54 clones and named core promoter deletion (CPD). CPD may have an important role in the cause of HBeAgnegative CHB. In addition, a novel deletion mutation in the X gene was observed in patients with CHB. This deletion mutant codes a 76aminoacid X factor instead of the X protein. In the present study, a new mutation pattern was discovered that may contribute to the cause of HBeAg-negative CHB, and therefore it is worthy of future studies.
Subject(s)
Hepatitis B e Antigens/blood , Hepatitis B virus/metabolism , Hepatitis B, Chronic/genetics , Trans-Activators/genetics , Adult , Amino Acid Sequence , DNA, Viral/chemistry , Female , Hepatitis B, Chronic/metabolism , Hepatitis B, Chronic/pathology , Humans , Male , Middle Aged , Molecular Sequence Data , Mutation , Promoter Regions, Genetic , Viral Regulatory and Accessory ProteinsABSTRACT
AIM: To study the role of mitochondrial energy disorder in the pathogenesis of ethanol-induced gastric mucosa injury. METHODS: Wistar rats were used in this study. A gastric mucosal injury model was established by giving the rats alcohol. Gross and microscopic appearance of gastric mucosa and ultrastructure of mitochondria were evaluated. Malondiadehyde (MDA) in gastric mucosa was measured with thiobarbituric acid. Expression of ATP synthase (ATPase) subunits 6 and 8 in mitochondrial DNA (mtDNA) was determined by reverse transcription polymerase chain reaction (RT-PCR). RESULTS: The gastric mucosal lesion index was correlated with the MDA content in gastric mucosa. As the concentration of ethanol was elevated and the exposure time to ethanol was extended, the content of MDA in gastric mucosa increased and the extent of damage aggravated. The ultrastructure of mitochondria was positively related to the ethanol concentration and exposure time. The expression of mtDNA ATPase subunits 6 and 8 mRNA declined with the increasing MDA content in gastric mucosa after gavage with ethanol. CONCLUSION: Ethanol-induced gastric mucosa injury is related to oxidative stress, which disturbs energy metabolism of mitochondria and plays a critical role in the pathogenesis of ethanol-induced gastric mucosa injury.
