Objective To observe the effects of Huazhuo Granule on expression of phosphatidylinositol-3-kinase (PI-3K) and glucose transporter 4 (GLUT4) in skeletal muscle type 2 diabetes (T2DM) rats;To discuss its effects on activating signal path of PI-3K and GLUT4. Methods High-fat diet combined with low-dose streptozotocin intraperitoneal injection was used to establish T2DM rat models. The rats were randomly divided into blank group, Huazhuo Granule group, rosiglitazone group, and model group. Each treatment group was given relevant medicine for gavage. Model group and blank control group were given normal saline for gavage. The general state, weight, and food ration of rats were observed. After ten-week medicine intervention, 10%chloral hydrate was used for anesthesia to detect the levels of FBG, OGTT (2 h PG), and FINS. RT-PCR was used to detect the expressions of PI-3K and GLUT4 mRNA of rat skeletal muscle in all groups. Results Compared with model group, the levels of FBG, 2 h PG, and FINS decreased (P<0.05);the expressions of PI-3K and GLUT4 mRNA of rat skeletal muscle increased significantly (P<0.05). Conclusion Huazhuo Granule has the effects on increasing insulin sensitivity, which is related to activating insulin signal path of PI-3K and GLUT4 of skeletal muscle tissues.

Objective To observe the effects of modified Liujunzi Decoction on improving isletβ-cell function of patients with the syndrome of spleen-deficiency and phlegm-stagnation of type2 diabetes mellitus.Methods Totally 72 patients were selected and divided into treatment group and control group randomly, with 36 cases in each group. Both groups were under diet adjustment and appropriate exercise and were given metformin hydrochloricle tablets, 0.5 g each time (1.0 g each time after 2 weeks), twice a day; acarbose, 50 mg each time, three times a day. The treatment group was given modified Liujunzi Decoction additionally, 200 mL each time, three times a day, orally. The course of treatment of the two groups was three months. Blood glucose, C peptide, INS, HbA1c, HOMA-IR, HOMA-β andΔI30/ΔG30 after 30 minutes of glucagon loading was recorded.Results Compared with before treatment, FBG, 30 min PBG, 2h PBG, HbA1c, FINS, fasting C-peptide, and HOMA-IR decreased in both groups, and the 30 min INS, 30 min C peptide, andΔI30/ΔG30 increased in the treatment group, with statistical significance (P<0.05). After treatment, there was statistical significance in FBG, 30 min PBG, 2 h PBG, HbA1c, fasting C-peptide, FINS, 30 min INS, 30 min C peptide, HOMA-IR, andΔI30/ΔG30 between the two groups (P<0.05).Conclusion Modified Liujunzi Decoction combined with Western medicine can better improve isletβ-cell function of patients with the syndrome of spleen-deficiency and phlegm-stagnation of type2 diabetes mellitus than Western medicine merely.

Female ; Humans ; Infant, Newborn ; Mouth ; microbiology ; Pregnancy ; Premature Birth ; microbiology

Objective:To construct specific small interfering RNA(siRNA) expressing vectors of intracellular Ca2+ transport protein(CaT1)gene and detect its silencing effects.Methods:The hairpin sequences of siRNAs targeting CaT1 gene were designed,synthesized and cloned into pSlincer 3.1-H1 plasmids after annealing.The vectors were then enriched in E.coli.The recombinant pSlincer 3.1-H1 plasmids were identified by restriction endonuclease cutting and DNA sequencing and then transfected into Human Gastric Carcinoma Cell Line BGC-823.The expression of CaT1 mRNA was examined by RT-PCR.Results:The siRNA oligonucleotides of CaT1 were correctly cloned into the pSlincer 3.1-H1 plasmids and confirmed by restriction endonuclease cutting and DNA sequencing.RT-PCR analysis revealed that the expression of CaT1 mRNA in BGC-823 cells transfected with the pSlincer 3.1-H1 constructs of siRNA was significantly decreased compared with that of the negative control and untransfected group.Conclusion:siRNA expression plasmids for silencing Ca2+ transport protein gene are successfully constructed,and they effectively inhibit the CaT1 gene expression.

Objective: To investigate the clinical value of two-dimensional speckle tracking echocardiography(2D-STE) combined with high-sensitive cardiac troponin T (hs-cTnT) in early detection of the cardiotoxicity induced by chemotherapy drug. Methods: Seventy-five non-Hodgkin′s lymphoma patients who received the CHOP regimen were recruited in this study. Conventional echocardiography and 2D-STE were performed on these patients before chemotherapy, the second day after the third course of chemotherapy (during chemotherapy) and the second day after the last course of chemotherapy (after chemotherapy). The parameters included left ventricular ejection fraction (LVEF), global longitudinal strain (LS), global circumferential strain (CS) and global radial strain (RS). The serum hs-cTNT levels were tested simultaneously. Results: Three cycles of CHOP were completed in 30 patients and 6-8 cycles of CHOP were completed in 45 patients. The LVEF of 75 patients before, during and after chemotherapy was (63.8±2.6)%, (63.8±2.8)% and (64.0±3.3)%, respectively, without significant difference (P=0.91). However, the LS of 75 patients before, during and after chemotherapy was (-18.5±1.7)%, (-16.5±1.9)% and (-16.0±1.6)%, respectively. The CS was (-20.9±2.9)%, (-19.3±3.5)% and (-19.2±3.2)%, respectively. The RS was (39.2±6.4)%, (35.3±5.2)% and (35.0±6.2)%, respectively. The hs-cTnT was (0.001 0±0.002 0)ng/ml, (0.006 3±0.008 9)ng/ml and (0.007 3±0.003 8)ng/ml, respectively. The LS, CS and RS were significantly decreased while hs-cTnT was significantly increased during chemotherapy when compared to those before chemotherapy (all of P<0.01). Alternatively, the LS, CS, RS and hs-cTnT after chemotherapy were marginally different from those during chemotherapy (all of P>0.05). Moreover, T_LS-SD, T_CS-SD and T_RS-SD showed no significant difference before, during and after chemotherapy (all of P>0.05). The reduction of LS was positively associated with the enhancement of hs-cTnT after chemotherapy (r=0.60, P<0.01). Conclusion 2D-STE combined with hs-cTnT can effectively and precisely detect the occult cardiotoxicity induced by anthracycline.

OBJECTIVE：To study the pr otective effect of schisandrin A （SA）on CCl 4-induced liver fibrosis model mice and its mechanism. METHODS ：Mice were randomly divided into blank control group ，model group ，silymarin group （positive control，100 mg/kg），SA low-dose and high-dose groups （20，40 mg/kg），with 10 mice in each group. Except for blank control group，other groups were given CCl 4 subcutaneously to induce liver fibrosis model. After successful modeling ，administration groups were given relevant medicine intragastrically ，once a day ，for consecutive 6 weeks；blank control group and model group were given constant volume of 0.5％sodium carboxymethyl cellulose solution intragastrically by the same way. HE staining was used to observe the pathological changes of liver tissue in mice. UV spectrophotometry and ELISA assay were adopted to detect the serum levels of liver injury indexes （ALT and AST ）and the contents of inflammatory factors （TNF-α，IL-1β，IL-6）. Western blotting assay was used to detect the expression of NOD like receptor protein 3（NLRP3）/NF-κB and TGF-β/Smad signaling pathway protein. RESULTS ：Compared with blank control group ，obvious pathological changes of liver fibrosis were observed in model group. The serum levels of liver injury indexes and contents of inflammatory factors were significantly increased （P＜0.01）. The expression of NLRP 3，apoptosis associated spot-like protein ，Caspase-1 and IL- 1β，TGF-β1 and ratios ofp-NF-κB p65/NF-κB p65，p-IκBα/IκBα，p-Samd3/Smad3 were increased significantly （P＜0.01）. Compared with model group ，SA could significantly relieve hepatic fibrosis in mice ，reduce serum levels of liver injury indexes and contents of inflammatory factors ，as well as the expression of NLRP 3/NF-κB and TGF-β/Smad signaling pathway protein and phosphorylation level（P＜0.01）. CONCLUSIONS ： SA can effectively relieve liver injury and inflammation of CCl 4-induced hepatic fibrosis model mice ，which may be through the regulation of NLRP 3/NF-κB and TGF-β/Smad3 signaling pathways ，thus inhibiting the process of liver fibrosis.