One hundred and sixty-two low back pain cases due to intervertebral disc problem were treated by puncturing 30 mm in depth with even reinforcing and reducing manipulation on Jiaji points (Ex-B 2) in the lumbar area plus patterned oral herbal decoction, Tao Hong Siwu Decoction. The result showed that 65 cases got marked effect, 53 cases got good effect, 37cases got certain effect, 6 cases got no effect and the total effective rate was 96.3%.

BACKGROUND:Acute pancreatitis is a common inflammatory disease mediated by pancreatic acinar cel s injury, and is mainly characterized by leukocyte infiltration. N-acetylcysteine can control leukocyte migration and regulate inflammation in some serious inflammatory diseases. OBJECTIVE:To investigate the protective effects of N-acetylcysteine in rat model of acute pancreatitis caused by sodium taurocholate. METHODS:Ninety Sprague-Dawley rats were randomly divided into three groups:normal control group, acute pancreatitis group and N-acetylcysteine group. Except normal control group, acute pancreatitis model was established in the other two groups by retrograde injection of sodium taurocholate into major duodenal papil a. Rats in the N-acetylcysteine group were treated with N-acetylcysteine intravenously through the tail vein. RESULTS AND CONCLUSION:After acute pancreatitis model was established, plasma amylase levels in the models were significantly higher than that in the normal control rats (P<0.05). Interleukin-1β,-6,-10, and tumor necrosis factorαexpression levels were also obviously higher than that in the normal control rats (P<0.05). Immunohistochemical staining demonstrated that N-acetylcysteine was mainly expressed in the islet cel s, and the pancreatic expression of N-acetylcysteine was down-regulated at both the mRNA and protein levels during the course of acute pancreatitis. N-acetylcysteine administration significantly reduced plasma amylase levels, myeloperoxidase activity, pro-inflammatory cytokine production, and pancreas and lung tissue damages. Furthermore, N-acetylcysteine administration did not cause significant inhibition of nuclear factor-κB activation in the pancreas. N-acetylcysteine is capable of improving damage of pancreas and lung, and exerting anti-inflammatory effects in rats with severe acute pancreatitis.