Objective To observe the TCM syndromes of acute exacerbation of chronic obstructive pulmonary disease (COPD) with malnutrition. Methods TCM Syndromes Questionnaire of Acute Exacerbation of COPD was formulated with TCM clinical epidemiology methods. Totally 220 cases of hospitalized patients met the inclusion criteria were divided into two groups, 120 cases of malnutrition and 100 cases of non-malnutrition. The clinical data were observed and syndrome elements of malnutrition group and non-malnutrition group were analyzed to discuss the rule of syndromes in acute exacerbation period. Results In addition to respiratory system, the frenquency of symptoms such as weight loss, shortness of breath, easy cold, aversion to wind and cold, poor appetite, abdominal distension, constipation, belching, dizziness and tinnitus, tooth loose and hair loss, soreness and weakness of waist and knees significantly increased in COPD with malnutrition, mainly involving in syndromes of spleen deficiency and incoordination between spleen and stomach. In patients with acute exacerbation of malnutrition COPD, the single syndromes were 36 cases (30%), the composite syndromes were 84 cases (70%). The simple excess syndromes were 38 cases (31.67%), the simple deficiency syndromes were 23 cases (19.17%), and the intermingled deficiency and excess syndromes were 59 cases (49.17%). Conclusion Patients with acute exacerbation of COPD with malnutrition are mainly composite syndromes and the intermingled deficiency and excess syndromes. Spleen deficiency and incoordination between spleen and stomach may be the important pathogenesis of COPD with malnutrition.

OBJECTIVE: To explore the role of mitochondrial permeability transition pore (mPTP) in mediating the protective effect of gastrodin against oxidative stress damage in H9c2 cardiac myocytes. METHODS: H9c2 cardiac myocytes were treated with HO, gastrodin, gastrodin+HO, cyclosporin A (CsA), or CsA+gas+HO group. MTT assay was used to detect the survival ratio of H9c2 cells, and flow cytometry with Annexin V-FITC/PI double staining was used to analyze the early apoptosis rate after the treatments. The concentration of ATP and level of reactive oxygen species (ROS) in the cells were detected using commercial kits. The mitochondrial membrane potential of the cells was detected with laser confocal microscopy. The expression of cytochrome C was detected with Western blotting, and the activity of caspase-3 was also assessed in the cells. RESULTS: Gastrodin pretreatment could prevent oxidative stress-induced reduction of mitochondrial membrane potential, and this effect was inhibited by the application of CsA. Gastrodin significantly lowered the levels of ROS and apoptosis-related factors in HO-exposed cells, and such effects were reversed by CsA. CsA significantly antagonized the protective effect of gastrodin against apoptosis in HO-exposed cells. CONCLUSIONS Gastrodin prevents oxidative stress-induced injury in H9c2 cells by inhibiting mPTP opening to reduce the cell apoptosis.
Adenosine Triphosphate ; analysis ; Apoptosis ; drug effects ; Benzyl Alcohols ; antagonists & inhibitors ; pharmacology ; Caspase 3 ; analysis ; Cell Line ; Cell Survival ; drug effects ; Cyclosporine ; pharmacology ; Cytochromes c ; analysis ; Glucosides ; antagonists & inhibitors ; pharmacology ; Humans ; Hydrogen Peroxide ; antagonists & inhibitors ; pharmacology ; Membrane Potential, Mitochondrial ; drug effects ; Mitochondrial Membrane Transport Proteins ; physiology ; Myocytes, Cardiac ; drug effects ; metabolism ; Oxidative Stress ; Reactive Oxygen Species ; analysis