Achalasia is a rare motor disorder of the esophagus and its etiology and pathogenesis remain unclear. Its clinical presentation typically includes various degrees of dysphagia, regurgitation, aspiration, chest pain and weight loss. The main therapy purpose for achalasia is to reduce lower esophageal sphincter pressure (LESP) so as to alleviate clinical symptoms. There are a variety of treatment methods for achalasia, such as pharmacotherapy, intrasphincteric botulinum toxin injection, endoscopic pneumatic dilatation and surgical intervention. At present, most scholars prefer laparoscopic or thorascopic surgery to achieve satisfactory long-term results including alleviated symptoms and prevention of acid reflux. However, great controversy still exists among scholars regarding the choice of conservative therapy or surgery, transthoracic or transabdominal surgery, optimal distal extent of myotomy, the need and choice of additional antireflux procedures. In this review, we focus on current therapy and progress of achalasia.
ObjectiveTo study the influence of myxobacteria metabolites NX52 and NX83 on the proliferation of colorectal carcinoma cells and investigate its probable mechanism. MethodsThe human colorectal carcinoma cell lines HT-29, SW480, and SW1463 were respectively treated with the two metabolites (NX52 and NX83) at different concentrations (0.1 mg/mL, 1.0 mg/mL, and 10.0 mg/mL), the cells of negative control were treated without metabolite. The proliferation inhibition was examined by methyl tthiazolyl tetrazolium assay. The cell morphology character was compared by inverted microscope, and the apoptosis of cell was analyzed by flow cytometry. ResultsTwo kinds of metabolites NX52 and NX83 had time-dose inhibitory effects on proliferation of human colorectal carcinoma cells HT-29, SW480, and SW1463 (P < 0.05). The metabolite NX83 had more obvious proliferation inhibition in the colorectal carcinoma cells as compared with the metabolite NX52 (P < 0.05). After 48 h, the apoptosis rate of the metabolite NX83 for SW1463 cell was observably increased as compared with the negative control group (P < 0.01). ConclusionsThe two kinds of metabolites NX52 and NX83 from myxobacteria could kill colorectal carcinoma cells in vitro. The possible mechanism might be induced by apoptosis of tumor cells.