ABSTRACT
The internal organs and meridians were associated with Yin and Yang, five elements, six qi, and time and space, based on the holistic view of heaven, earth and human, according to Huangdi Neijing. The syndrome differentiation system of six meridians and Zang Fu meridians were established by Shanghan Zabing Lun, on the basis of the three Yin, three Yang, six meridians, and five Zang system in Huangdi Neijing. We put forward the concept of the six meridians syndrome differentiation system of circular motion, considering that the six meridians syndrome differentiation system actually implies the theory of circular motion. The syndrome differentiation system was constructed with the circular model of one qi circulating around the road, rising left and falling right, corresponding up and down, and maintaining conservation in the middle as the core, integrating Yin and Yang, five elements, six qi, Zang Fu and meridians, qi, blood and body fluid, and the integration of heaven, earth and human, focusing on "disease location and disease nature", taking classical prescriptions as the main treatments, and cooperating with external treatments such as acupuncture and moxibustion. We organically combined the circular motion with the syndrome differentiation of the six meridians, systematically interpreted the physiological bases, pathological changes, progressive patterns, and the treatments, based on syndrome differentiation, by inheriting the classical thinking mode of Hetu, Luoshu,Zhouyi, Huangdi Neijing, ShennongHerbal Classic, and Shanghan Zabing Lun.
ABSTRACT
To investigate the effect of manganese superoxide dismutase (MnSOD) silence on the in vitro tumorigenicity in human small cell lung cancer NCI-H446 cells and the underlying mechanisms. Methods: Sphere formation cells from NCI-H446 cells were obtained by suspension culture, while the expression of MnSOD and urokinase type plasminogen activator (uPAR) was analyzed by Western blot. Silence of MnSOD was performed by adenovirus infection in the second passage formation cells, and the effect of MnSOD silence on tumorigenicity in NCI-H446 cells was evaluated by sphere formation assay and soft-agar colony formation assay, while the expression of uPAR was analyzed by Western blot. Results: Compared with NCI-H446 cells, the sphere formation rate, colony formation rate, and the expression of MnSOD and uPAR were significantly increased in the second passage sphere formation cells in NCI-H446 cells (P<0.05). Silence of MnSOD inhibited the sphere formation rate, colony formation rate, and the expression level of uPAR in the second passage sphere formation cells in NCI-H446 cells. Conclusion: MnSOD may promote tumorigenicity in NCI-H446 cells by up-regulation of uPAR expression in vitro.
Subject(s)
Humans , Adenoviridae , Carcinogenesis , Cell Line, Tumor , In Vitro Techniques , Lung Neoplasms , Metabolism , RNA Interference , Receptors, Urokinase Plasminogen Activator , Genetics , Metabolism , Small Cell Lung Carcinoma , Metabolism , Spheroids, Cellular , Pathology , Superoxide Dismutase , Genetics , Metabolism , Tumor Stem Cell Assay , Up-RegulationABSTRACT
To investigate the effect of apigenin on self-renewal for sphere-forming cells in human small cell lung cancer cell line NCI-H446 and the underlying mechanisms. Methods: Sphere-forming cells from NCI-H446 cell line were cultured in stem cell-conditioned culture medium with ultra-low attachment surface plates. The rate of sphere-forming cells in the second passage sphere-forming cells was used to evaluate the inhibitory effects of apigenin on the self-renewal for sphere-forming cells. The protein level of urokinase-type plasminogen activator receptor (uPAR) in spheroids was analyzed by Western blot. Results: Apigenin signifcantly inhibited the self-renewal of the second passage sphere-forming cells [0, 5.0, 10.0, 20.0 μmol/L apigenin: (18.2±1.9)%, (13.6±1.7)%, (10.6±1.6)%, (6.9±1.3)%, respectively] and down-regulated uPAR expression in a concentration-dependent manner (P<0.05). Conclusion: Apigenin inhibits the self-renewal capacity of sphere-forming cells in NCI-H446 cells, which may be associated with down-regulation of uPAR expression.
Subject(s)
Humans , Apigenin , Pharmacology , Cell Line, Tumor , Down-Regulation , Genetics , Lung Neoplasms , Neoplastic Stem Cells , Pathology , Physiology , Receptors, Cell Surface , Receptors, Urokinase Plasminogen Activator , Genetics , Metabolism , Signal Transduction , Small Cell Lung Carcinoma , Drug Therapy , Pathology , Spheroids, Cellular , Physiology , Stem CellsABSTRACT
Objective:To explore the effects of total saponins of Cornus offlcinalis Sieb.(TSCO) on the contractility and relaxation of mesenteric artery in streptozotocin (STZ)-induced diabetic rats.Methods:Sprague Dawley rats were administrated STZ intra-peritoneally at a dosage of 60 mg/kg to induce diabetes.TSCO was administrated at a dosage of 60 mg/kg or 120 mg/kg (per os) to the diabetic rats for 28 days.Glucose and insulin in the serum as well as the responsiveness ofmesenteric artery rings were determined.Results:TSCO decreased the contractile responsiveness to phenylephrine of mesenteric artery rings from diabetic rats,but increased the reactivity to acethylcholine.TSCO (120 mg/kg) ameliorated the baseline release of nitric oxide of mesenteric artery,but had little effect on the induced release of nitric oxide.Rosiglitazone had less effect on the mesenteric artery function than that of TSCO,though it was more effective on lowering blood glucose.Conclusion:The effects of TSCO on mesenteric artery of diabetic rats are dose dependent,and are possibly exerted by lowering blood glucose and ameliorating the release of nitric oxide in the endothelium.
ABSTRACT
OBJECTIVE@#To observe the relation between the expression of CTNNAL1 and the airway resistance in rats with airway hyperresponsiveness.@*METHODS@#Thirty Wister rats were randomly divided into 5 groups: a normal control group, a 2 d ozone attack group, a 4 d ozone attack group, a 6 d ozone attack group, and a 6 d ozone attack+2 d dexamethasone treatment group (6 rats in each group). The distribution of CTNNAL1 was observed by in situ hybridization; the expression of CTNNAL1 was detected by fluorescence quantitative RT-PCR; the airway resistance was detected in by Buxco pulmonary function analysis system; and the relevance of the expression of CTNNAL1 and the resistance of respiratory tract in rat with airway hyperresponsiveness were analyzed.@*RESULTS@#CTNNAL1 was distributed in bronchial epithelial cells, goblet cells, endothelial cells, and the alveolar wall. With the increase of the ozone attack, the expression of CTNNAL1 mRNA gradually reduced, the airway hyperresponsiveness was aggravated, and the airway resistance was increased.@*CONCLUSION@#During airway hyperresponse, the reduction of CTNNAL1 mRNA can increase the airway resistance. There is a negative correlation between the reduction of CTNNAL1 mRNA and the airway hyperresponsiveness. CTNNAL1 is an adhesion molecule related to airway hyperresponsiveness susceptibility.
Subject(s)
Animals , Female , Male , Rats , Airway Resistance , Bronchial Hyperreactivity , Metabolism , Inflammation , Ozone , RNA, Messenger , Genetics , Metabolism , Rats, Wistar , alpha Catenin , Genetics , MetabolismABSTRACT
Objective:To observe the protective effects of sodium ferulate (SF) on rabbit myocardial ischemia reperfusion injury. Method: Sixteen rabbits were divided randomly into three groups: group A undergoing all procedures except for ischemia-reperfusion and treatment, group B given the routine treatment after ischemia-reperfusion, and group C receiving the routine treatment combined with the intravenous infusion of SF 40mg?kg~(-1) after ischemiareperfusion. Result: Group C showed a significant reduction in myocardial MDA content and plasma ET level (P