ABSTRACT
<p><b>OBJECTIVE</b>To investigate the therapeutical effects of KANGFUXINYE on the upper gastrointestinal injury induced by paraquat in rats, and to explore the proper mechanism.</p><p><b>METHODS</b>A total of 120 adult Wistar male rats were randomly divided into three groups, control group (CG), model group (MG) and treatment group (TG), 40 rats each group. The MG and TG were given 20% paraquat 50 mg/kg by oral administration, after 2 h the TG was given KANGFUXINYE solution 1.5 ml by oral administration, 3 times a day. The CG was given normal saline. On the 3rd, 6th, 9th, 12th and 15th days after exposure, 8 rats of each group were killed respectively, and the tissues from esophagus and stomach were collected and examined by HE staining for observing the mucosa injury. The superoxide dismutase (SOD) and malondialdehyde (MDA) of serum were detected.</p><p><b>RESULTS</b>On the 3rd, 6th, 9th, 12th and 15th days after exposure, the results of pathological examination showed that the mucosa injury in TG was significantly relieved as compared with MG, the activity of serum SOD reduced obviously and the MDA levels increased significantly in MG, as compared with CG (P<0.05). The activity of serum SOD increased obviously and the MDA levels decreased significantly in TG, as compared with MG (P<0.05).</p><p><b>CONCLUSION</b>The results of present indicate that KANGFUXINYE has the therapeutical effects on the upper gastrointestinal injury caused by paraquat in rats. The mechanism of therapeutical effects may be due to the increasing SOD activity, eliminating free radicles and inhibiting the lipid peroxidation.</p>
Subject(s)
Animals , Male , Rats , Biological Products , Therapeutic Uses , Disease Models, Animal , Gastrointestinal Diseases , Metabolism , Therapeutics , Lipid Peroxidation , Malondialdehyde , Metabolism , Paraquat , Poisoning , Rats, Wistar , Superoxide Dismutase , MetabolismABSTRACT
<p><b>OBJECTIVE</b>To investigate the clinical therapeutic effect of methylprednisolone combined with cyclophosphamide and Etanercept method on acute paraquat poisoning.</p><p><b>METHODS</b>136 patients with acute paraquat poisoning were divided into the normal therapy group and the intensive therapy group randomly. Methylprednisolone, cyclophosphamide and Etanercept were used in the intensive therapy group. Methylprednisolone 500 mg was given intravenously per day for continuous three days followed by 200 mg intravenous per day. Then methylprednisolone was decreased gradually 14 d or 21 d later according to the patient's condition. Cyclophosphamide 600 mg was given intravenously twice weekly for 2 weeks and Etanercept 25 mg was given hypodermic injection twice weekly for 3 weeks. Curative effect evaluation was done at 7, 14, 21 d and 12 weeks after therapy.</p><p><b>RESULTS</b>The survival rate of the intensive therapy group was obviously higher than that of the normal therapy group (P<0.01) on 7, 4, 21 d and 12 weeks. The cure rate of the intensive group were 94.6% (intake dose<50 ml 20% paraquat solution), 75.0% (intake dose 50 approximately 100 ml 20% paraquat solution), 12.5% (intake dose>100 ml 20% paraquat solution) respectively, while the cure rate of the normal group were 16.7% (intake dose<50 ml 20% paraquat solution), 8.3% (intake dose 50 approximately 100 ml 20% paraquat solution), 0% (intake dose>100 ml 20% paraquat solution) respectively. The total cure rate of the intensive therapy group (78.3%) 12 weeks later was higher than that of the normal group (11.9%).</p><p><b>CONCLUSION</b>Methylprednisolone combined with cyclophosphamide and Etanercept intensive therapy has the curative effect on acute paraquat poisoning.</p>
Subject(s)
Adolescent , Adult , Female , Humans , Male , Middle Aged , Young Adult , Acute Disease , Cyclophosphamide , Therapeutic Uses , Drug Therapy, Combination , Etanercept , Immunoglobulin G , Therapeutic Uses , Methylprednisolone , Therapeutic Uses , Paraquat , Poisoning , Poisoning , Drug Therapy , Receptors, Tumor Necrosis Factor , Therapeutic Uses , Treatment OutcomeABSTRACT
RASSF1A gene cloned from 3p21.3 region is a novel candidate tumor suppressor gene. The aberrant methylation of CpG lands in the promoter region is the major inactivation mechanism of RASSF1A, and is significantly involved in the genesis and development of multiple solid tumors including prostate cancer. The methylation status examination of RASSF1A could serve as an important technique for the early diagnosis of prostate cancer, while methylation inhibitor is likely to become a novel therapeutic agent.
