Objective To explore the clinical efficacy and safety of nicorandil in the treatment of chronic ischemic cardiomyopathy patients with heart failure. Methods The chronic ischemic cardiomyopathy patients with heart failure in our hospital were divided into two groups according to the random number table method. Control group underwent conventional anti heart failure treatment and symptomatic supportive treatment , and treatment group was treated by the nicorandil in addition to above treatments. After treatment for 6 months , comparisons of clinical efficacy and safety between two groups were conducted. Results The improvement of heart function in observation group was better than that in control group (Z = -2.302, P = 0.021). After treatment, the LVEF, 6 min walking distance were greater than those before treatment, and the LVESD, LVEDD were less than those before treatment (P < 0.05). The LVEF, 6 min walking distance in observation group after treatment were greater than those in control group and the LVESD , LVEDD were less than those in control group (P < 0.05). The incidence rate of adverse reaction in observation group was 9.59%, and 6.94% in control group, without statistical difference between two groups (χ2 = 0.334,P = 0.563). Conclusion In addition to conventional anti heart failure treatment , nicorandil can significantly improve the curative effect and the heart function in the treatment of chronic ischemic cardiomyopathy patients with heart failure and there are no significant adverse reactions. In addition , patients are tolerant.

Objective To observe the prevention and treatment of the total flavonoids from Litchi chinensis Sonn( TFL) on hepatic fibrosis induced by dimethylnitrosamine(DMN)in rats, and to explore its mechanism. Methods Ninety SD rats were randomly divided into six groups, normal control group, model control group, colchicine group, high-, medium- and low-dose TFL group(n=15).Expect for normal control group, the other groups were given intraperitoneal injection of 2 mL.kg-1 of 5% dimethylnitrosamine for 4 weeks as the model group. The rats in the normal control group and model control group were given 5 mL.kg-1of 0.9% sodium chloride solution, colchicine group was treated with 0.1 mg.kg-1 colchicine.High-, medium-and low-dose TFL groups were given 200, 100 and 50 mg.kg-1 of TFL.The rats were sacrificed and the livers were harvested and stained with HE and Masson staining to observe pathological changes and liver fibrosis in the same part 6 weeks after all the medicine was given to the rats each day. Immunohistochemistry and Western blotting were used to detect the expression of the transforming growth factor β-Ⅰ/type Ⅱ receptor ( TβRⅠ/Ⅱ) , collagen Ⅰ( Col Ⅰ) and Ⅲ collagen ( Col Ⅲ) . Results Compared with the normal control group, the semiquantitative score of liver fiber and the protein expression of TβRⅠ, TβRⅡ, ColⅠ and Col Ⅲ in the model control group were significantly increased(P<0.01).Compared with the model control group, the protein expression levels of TβR, TβRⅡ, ColⅠand ColⅢwere significantly decreased( P<0.01) in the high-,medium-and low-dose TFL group.The semiquantitative score of liver fiber was significantly decreased( P<0.01) with a dose-effect relationship. Conclusion TFL can inhibit formation of DMN-induced liver fibrosis in rats, which may be related with reduction of expression of TβRⅠ/Ⅱ of hepatic fibrosis promoting factor TGF-β1 , inhibition of the activation and increase of hepatic stellate cells, reduction of the collagen content.

Objectives To analyze the expression of fibroblast growth factor-19(FGF-19) in hepatocellular carcinoma ( HCC) and adjacent tissues , and to investigate its clinical significance .Methods A total of 209 HCC patients who had undergone radical resection operations at Hospital 401 between January 2003 and December 2009 were chosen as samples . Immunohistochemistry method was employed to examine the expression level of FGF-19 in HCC and adjacent tissues .The relationship between FGF-19 protein expressions and clinicopathological features was analyzed by the chi -square test or Fisher exact probability .A survival curve was drawn using the Kaplan-Meier method and the Cox model was used to analyze factors that influenced survival .Results The rate of high expression of FGF-19 was 66.1% (138/209) in HCC, which was significantly higher than 46.9%(98/209) in adjacent tissues (P<0.05).The high expression of FGF-19 was related to the tumor capsule and tumor boundary (P<0.05).The overall survival in high expression of FGF-19 group was signifi-cantly lower than that in low expression group (P<0.05).Conclusion FGF-19 plays an important role in the carcinogen-esis and development of HCC , and a high expression of FGF-19 might be closely related to survival time of postoperative patients.FGF-19 might be a potential prognosis prediction factor for HCC .

Objective To investigate effects of total flavonoids of litchi (TFL) on the proliferation of rat hepatic stellate cells (HSC-T6) in comparison with western medicine rosiglitazone, and to explore the mechanism of anti hepatic fibrosis of TFL. Methods Effect of TFL on proliferation of HSC-T6 was examined by MTT. The expression of peroxisome proliferator-activated receptor-γ (PPAR-γ) mRNA, connective tissue growth factor (CTGF) mRNA in HSC-T6 cells exposured were examined by real-time quantitative PCR. Effects on HSC-T6 CTGF protein from TFL and rosiglitazone were detected by Western bloting. Results The expression of PPAR-γ mRNA was upregulated and the expression of CTGF mRNA and protein was downregulated after exposure to TFL and rosiglitazone for 72 hours. And the effect of TFL increased with the increase of concentration. Conclusion TFL can inhibit the proliferation of HSC-T6 and antagonizing liver fibrosis. This mechanism may be associated with the upregulation of PPAR-γ expression and the downregulation of CTGF expression.

Aim To investigate the effects of ursolic acid from loquat leaves on proliferation inhibition and expression of PPAR-γ 、TGF-β1 in rat hepatic stellate cells, so as to explore the mechanism of anti-hepatic fibrosis of UA.Methods HSC-T6 cells were randomly divided into blank group, rosiglitazone control group, the low, medium and high concentration of UA group to detect the cell proliferation inhibition by CCK-8 after 24,48,72 h.The content of type collagen Ⅰ in cell culture supernatant of each group was examined by ELISA.The expression of PPAR-γ mRNA, TGF-β1 mRNA in HSC-T6 cells exposured were examined by real-time quantitative PCR.Effects on HSC-T6 PPAR-γ and TGF-β1 protein from each group were detected by immunocytochemical method.Results CCK-8 results showed that the inhibitory rate of UA on cell proliferation increased with the prolongation of drug action time(P<0.01).ELISA results showed that with the increase of the concentration of UA, the content of type Ⅰ collagen content decreased(P<0.01).Real-time PCR results showed that with the increase of the concentration of UA, and the expression of PPAR-γ mRNA increased, the expression of TGF-β1 mRNA decreased(P<0.01).The results of immunocytochemistry showed that the expression of PPAR-γ protein was increased, and the expression of TGF-β1 protein was decreased with the increase of the concentration of UA(P<0.01).All effects mentioned above were dose-dependent.Moreover, the effects in the high concentration groups were stronger than those in control group.Conclusion UA can inhibit the proliferation of HSC-T6 cells, Which may be associated with the up-regulation of PPAR-γ expression and the down-regulation of TGF-β1 expression.

Objective: To analyze implant survival rate and incidence rate of complications after All-on-4 implantation, and to discuss the technical points and consideration of All-on-4. Methods : According to the criteria of inclusion and exclusion, 23 cases treated with All-on-4 immediate restoration were referred, from January 2007 to December 2015, including 5 cases of edentulous maxillary, 14 cases of edentulous mandibular and 4 cases of both maxillary and mandibular were edentulous. All the patients received immediate function with provisional prostheses at the surgery day. Definitive prostheses were delivered to patients after 3-6 months post operation and follow-up visits were performed up to 9 years (average 3 years) after placement of definitive prostheses. Results : In this study, the rate of implant retention of 108 implants and 27 final restorations was 100% until the last review. Among the 23 patients, 3 patients had complications and the incidence of complications was 13.0%. Conclusion All-on-4 is an effective and reliable method in the treatment of dentures denture. The incidence of complications is low. All-on-4 is a practical method.

ObjectiveTo study the effect of total flavone of Litchi Semen （TFL） on proliferation， apoptosis， migration， and invasion of hepatoma cells HepG2. MethodMethyl thiazolyl tetrazolium colorimetric （MTT） assay was used to detect the effect of different-dose TFL and cisplatin on the proliferation of HepG2 cells. TdT-mediated dUTP nick-end labeling （TUNEL） assay was used to detect the effects of low， medium， and high-dose （70， 140， 210 mg·L^-1） of TFL and cisplatin （60 mg·L^-1） on the apoptosis of HepG2 cells， thus selecting the optimal dose of TFL for the follow-up experiment. HepG2 cells were divided into a blank group， a TFL group （140 mg·L^-1）， a TFL+XL019 group （140 mg·L^-1 TFL+0.5 μmol·L^-1 XL019）， and a TFL+TPI-1 group （140 mg·L^-1 TFL+1 μmol·L^-1 TPI-1）. The effect of TFL on migration and invasion of HepG2 cells were examined by wound healing test and Transwell invasion assay， and the effect of TFL on the expression of epithelial-mesenchymal transition （EMT） marker in HepG2 cells were examined by cell immunofluorescence assay. Western blot was used to detect the expression of key proteins in Janus kinase 2（JAK2）/signal transducer and activator of transcription 3 （STAT3） signaling pathway after the intervention by TFL. ResultMTT assay showed that the proliferation of HepG2 cells was significantly inhibited by TFL and cisplatin at 24 and 48 h as compared with blank group （P<0.01）， and the half maximal inhibitory concentration （IC₅₀） of TFL on HepG2 cells was （136.7±2.40） mg·L^-1 at 24 h and （106.8±1.11） mg·L^-1 at 48 h. The IC₅₀ of cisplatin on HepG2 cells was （58.48±2.04） mg·L^-1 at 24 h and （5.15±0.56） mg·L^-1 at 48 h. The results of TUNEL assay showed that TFL induced apoptosis of HepG2 cells. The optimal dose of TFL was 140 mg·L^-1. The results of wound healing test showed that compared with the blank group， the TFL group， TFL+XL019 group， and the TFL+TPI-1 group significantly inhibited the migration of HepG2 cells （P<0.05， P<0.01）. As compared with the TFL group， the inhibitory effect of the TFL+XL019 Group was significantly increased （P<0.05）， while that of the TFL+TPI-1 group was significantly decreased （P<0.01）. The Transwell invasion assay showed that compared with the blank group， the TFL group， TFL+XL019 group， and the TFL+TPI-1 group significantly inhibited the invasion of HepG2 cells （P<0.01）. As compared with the TFL group， the inhibitory effect of the TFL+XL019 group was significantly increased （P<0.05）， while that of the TFL+TPI-1 group was significantly decreased （P<0.01）. The results of immunofluorescence showed the intervention of TFL up-regulated the expression of E-cadherin， and down-regulated the expression of Vimentin in HepG2 cells， which was stronger in the TFL+XL019 group and weaker in the TFL+TPI-1 group. The results of Western blot showed that compared with the blank group， the TFL group， TFL+XL019 group， and the TFL+TPI-1 group did not affect the expression of JAK2 or STAT3 protein， but significantly decreased the expression levels of phosphorylatied （p）-JAK2 and p-STAT3 （P<0.05， P<0.01）. As compared with the TFL group， the expression levels of p-JAK2 and p-STAT3 in the TFL+XL019 group were significantly decreased （P<0.01）， while those in the TFL+TPI-1 group were significantly increased （P<0.01）. Compared with the blank group， the TFL group significantly increased the expression level of Src-homology domain 2 containing protein tyrosine phosphatase-1（SHP-1） with sh2 domain （P<0.01）. ConclusionTFL has the effects of inhibiting the proliferation， promoting apoptosis of HepG2 cells， and reversing the EMT process of HepG2 cells to reduce the migration and invasion， which are presumably related to the activation of SHP-1 by TFL to block JAK/STAT3 signaling pathway.

Gastric cancer is a common malignant tumor of the gastrointestinal tract， with the pathogenesis remains to be fully elucidated. Although surgery， radiotherapy， chemotherapy， targeted therapy， and immunotherapy have demonstrated obvious clinical efficacy in the treatment of gastric cancer， the patients suffer from complications and adverse effects. Basic experiments and clinical studies have proved that Chinese medicine can treat gastric cancer in a multi-component and multi-target manner， the mechanisms of which remain to be deciphered. Therefore， the mechanism of Chinese medicine against gastric cancer needs to be unveiled by network pharmacology and tools of molecular biology. According to Chinese medicine， the occurrence of gastric cancer is mainly attributed to liver Qi stagnation， phlegm stasis and Qi stagnation， body fluid deficiency and heat accumulation， deficiency of healthy Qi， and cancer toxin accumulation. According to the available literature， herbal compound formulas such as Sancao Tiaowei decoction， Xiaojianzhong decoction， and Yiqi Huayu Jiedu decoction focus on tonifying， clearing heat， and detoxifying， while herbal active components are mainly insecticidal， heat-clearing， blood-activating， stasis-removing， and Qi-regulating drugs. The therapeutic effects of these Chinese medicines are consistent with the etiology and pathogenesis of gastric cancer. It has been demonstrated that Chinese medicines play a role in promoting apoptosis and autophagy， blocking cell cycle， and reversing cellular drug resistance to treat gastric cancer by regulating phosphatidylinositol-3 kinase/protein kinase B （PI3K/Akt）， mitogen-activated protein kinase （MAPK）， nuclear factor-kappa B （NF-κB）， transforming growth factor-β （TGF-β）/Smad， Wnt/β-catenin， and Hedgehog signaling pathways， while there is a lack of systematic understanding. By systematically summarizing the signaling pathways related to the regulation of gastric cancer by Chinese medicine， this study aims to clarify the molecular mechanisms of Chinese medicine against the development， invasion， and metastasis of gastric cancer， with a view to providing new targets， perspectives， and ideas for the treatment of gastric cancer and promoting the modernization of traditional Chinese medicine.

Objective To investigate the effect and mechanism of Shuangzhu Kangxian Prescription(Astragali Radix,bran-fried Atractylodis Macrocephalae Rhizoma,vinegar-prepared Rhizoma Curcumae,Bupleuri Radix,Salviae Miltiorrhizae Radix et Rhizoma,Litchi Semen)on improving hepatitic fibrosis induced by carbon tetrachloride(CCl4)in rats based on the Wnt/β-catenin signaling pathway.Methods The rat model of hepatitic fibrosis was replicated by subcutaneous injection of 3.0 mL·kg-1 40%CCl4 twice a week for 8 weeks.SD rats were randomly divided into blank control group(n=8),model group(n=7),positive control group(n=7,intragastric administration of 43.19 mg·kg-1 silymarin),low-dose Chinese medicine group(n=6,intragastric administration of 4.3 g·kg-1Shuangzhu Kangxian Prescription),medium-dose Chinese medicine group(n=6,intragastric administration of 8.6 g·kg-1Shuangzhu Kangxian Prescription),high-dose Chinese medicine group(n=7,intragastric administration of 17.2 g·kg-1Shuangzhu Kangxian Prescription).The continuous intragastric administration was given once a day for 4 consective weeks,in addition to the blank control group,the other groups continued to be subcutaneously injected with CCl4 at the same time.The pathological changes of liver tissue were observed by HE and Masson staining.The levels of serum type Ⅳ collagen(Col Ⅳ),type Ⅲ procollagen(PC Ⅲ),hyaluronic acid(HA)and laminin(LN)were detected by ELISA.The protein expression levels of Wnt1,β-catenin and PPAR-γ in liver tissue were detected by Western Blot.The mRNA expression levels of Wnt1,β-catenin and PPAR-γ in liver tissue were detected by qPCR.Results Compared with the blank control group,the liver of the model group showed partial necrosis of liver cells,the normal hepatic lobule structure was destroyed,the arrangement of liver cell cords was disordered,the central vein or portal area was enlarged,and a large number of inflammatory cells infiltrated to form bridging necrosis.The collagen fibers in the central vein or portal area of the liver proliferated significantly,forming fibrous septa,and the fibrosis score were significantly increased(P＜0.05).The levels of serum Col IV,PC Ⅲ,HA and LN were significantly increased(P＜0.05).The protein and mRNA expression levels of Wnt1 and β-catenin in liver tissue were significantly increased(P＜0.05),and the protein and mRNA expression levels of PPAR-γ were significantly decreased(P＜0.05).Compared with the model group,the steatosis of hepatocytes in the positive control group and the medium-and high-dose groups of Chinese medicine was improved,and the necrosis and inflammatory cell infiltration were reduced.The degree of hepatitic fibrosis was improved,the liver collagen fibers were reduced,and the fibrosis score was significantly reduced(P＜0.05).The levels of serum Col Ⅳ,PC Ⅲ,HA and LN were significantly decreased(P＜0.05).The protein and mRNA expression levels of Wnt1 and β-catenin in liver tissue were significantly decreased(P＜0.05),and the protein and mRNA expression levels of PPAR-γ were significantly increased(P＜0.05).Conclusion Shuangzhu Kangxian Prescription has the effect of anti CCl4-induced hepatitic fibrosis in rats,and its mechanism may be related to the inhibition of Wnt/β-catenin signaling pathway and up-regulation of PPAR-γ expression.

Humans ; Severe Acute Respiratory Syndrome ; diagnosis ; therapy