Objective To investigate the influence of salvianolic acid B on the expressions of TGF-β1/Smad signaling pathway related proteins in human lung fibroblasts,and to explore the mechanism of the inhibitory effect of Sal B on TGF-β1-induced lung fibroblast activation.Methods The human embryonic lung fibroblasts (MRC-5) were cultured in vitro and randomly divided into control group ( the cells were cultured with DMEM without TGF-β1 or Sal B),Sal B group (the cells were cultured with 10μmol·L-1 Sal B),TGF-β1 group (the cells were cultured with 10μg·L-1 TGF-β1),and TGF-β1 (10μg·L-1 )+ Sal B (10μmol·L-1 )group.The protein levels of p-Smad2,p-Smad3,TβRⅠ,and Smad7 in the fibroblasts in various groups were detected by Western blotting method.Results Compared with control group,the expression levels of p-Smad2,p-Smad3,and TβRⅠproteins in TGF-β1 group were significantly increased (P<0.05),and the expression level of Smad7 protein was decreased (P<0.05).Compared with control group,the expression levels of p-Smad2,p-Smad3,TβRⅠ,and Smad7 proteins in lung fibroblasts in Sal B group had no significant change (P>0.05).Compared with TGF-β1 group,the expression levels of p-Smad2,p-Smad3,and TβRⅠ in TGF-β1+ Sal B group were descended (P<0.05),and the expression level of Smad7 was increased (P<0.05).Conclusion Sal B could suppress the TGF-β/Smad signaling pathway in lung fibroblasts and to inhibit the TGF-β1-induced lung fibroblast activation.

Objective To investigate the therapeutic effects of Tongxinluo and its influence on the expression of CD40 and CD40L in artherosclerosis rabbits. Methods 60 male rabbits were divided into three groups randomly,20 of each group: normal control group, model group and Tongxinluo group. The rabbits in model group and Tongxinluogroup were used to prepare the atherosclerosis model induced by high-cholesterol diet. The levels of ET-1, NOwere measurde. Before and 12 weeks after durg treatment,serum total cholesterol ,plaque areas and ratios of intima/media thickness were detected. The expression of CD40 and CD40L mRNA were determinated by quantitive RT-PCR. Results Serum total cholesterol level of Tongxinluo group was decreased compared with model group ( P < 0. 05 ), and they were both much higher than those of normal control group ( P < 0. 01 ); as compared with the model group, aortic plaque areas and ratios of intima/media thickness in Tongxinluo group reduced significantly [ (0.56 ± 0. 07) vs ( 1.16±0.08),P<0.01;(36.88±2.38)% vs (76.58 ±2.86) %,P <0. 0l] ;The expression of CD40 and CD40L mRNA also decreased in Tongxinluo group with statistic significance[ (0.798 ± 0.115 )、 (0. 592 ± 0. 132) vs (0.686±0. 132) 、(0.498 ±0. 108) ,P <0. 01 ) ]. Conclusion Tongxinluo had the ability to anti-artherosclerosis and its possible mechanism was down-regulate the expression of CD40 and CD40L.

Objective To study the effect of matrine on ATP binding cassette transporter A1 (ABCA1) expression and cholesterol in monocyte derived foam cells. Methods The lipid peroxide in cells was measured by TBARS method; The foam cells were examined by oil red O stain. The accumulation of cholesterol in monocyte was measured by fluorescence spectrophotometric method;ABCA1 mRNA and its protein level were determined by RT-PCR and Western blot, respectively. Results In the homonocytes incubated with PMA and low density lipoprotein (LDL), the intracellular accumulated total cholesterol (TC), free cholesterol (FC), cholesteryl ester (CE) and lipid peroxide increased obviously, and a huge amount of foam cells were found by oil red O stain. This was accompanied by a reduction in the membrane content of ABCA1. matrine alter ABCA1 mRNA abundance, indicating that increased ABCA1 transcription, enhanced mRNA level.Conclusion The mechanism of anti-artherosclerosis by matrine may be related to reduce cholesterol and to increase the level of ABCA1 expression.

Objective To investigate primarily the correlation between depression and prognosis in patients with coronary heart disease(CHD).Methods 246 CHD patients were divided into the depression group and non-depression group.The relation between depression and incidence of short term cardiovascular events was compared.Results The incidence of angina pectoris,ST-segment elevated myocardial infarction,non ST-segment elevated myocardial infarction,congestive heart failure,ventricular tarchycardia,ventricular fibrillation and sudden death in the near future were 75.6%,11.1%,17.8%,26.7%,12.2%,8.9% and 7.8% respectively.Depression was an independent predictive factor of all cardiovascular events.Conclusion CHD patients complicated by depression have a high incidence of cardiovascular events,and the depression is an independent predictive factor of all cardiovascular events.

Objective:To explore the expression of family with sequence similarity 83 member A (FAM83A) in colorectal cancer, and the effect of FAM83A knockdown on the proliferation of colorectal cancer cells and the related mechanism.Methods:The expression of FAM83A in the tissues of 102 patients with colorectal cancer and its adjacent tissues was detected by immunohistochemistry. HCT116 cells were divided into experimental group and control group. The experimental group cells were transfected with FAM83A-siRNA plasmid, and the control group cells were transfected with MOCK-siRNA plasmid. The mRNA content of FAM83A in each group was detected by fluorescence quantitative PCR. The expressions of FAM83A, P13K, p-AKT and p-mTOR in each group were detected by Western blot. CCK8 assay and clonogenesis assay were used to detect cell proliferation.Results:The positive rate of FAM83A in colorectal cancer patients was 88.23% (90 cases /102 cases), and the expression rate of FAM83A in paracancer tissues was 10.78% (11 cases /102 cases). The expression rate of Fam83a in colorectal cancer tissues was significantly higher than that in paracancer tissues, with statistical significance ( P<0.001). After siRNA transfection, the mRNA expression levels of FAM83A in HCT116 cells of the experimental group and control group were 1.23±0.20 and 0.43±0.12, respectively, and the protein expression levels of FAM83A were 1.19±0.11 and 0.23±0.08, respectively. The expression levels of P13K were 1.21±0.17 and 0.28±0.09, the expression levels of p-AKT were 1.35±0.23 and 0.57±0.18, and the expression levels of p-mTOR were 1.48±0.20 and 1.05±0.14. The expression of P13K, p-Akt and p-mTOR was down-regulated (all P<0.05). The absorbance of HCT116 cells in the experimental group and the control group was 1.09±0.22 and 2.21±0.27, respectively. The cloning rate of HCT116 cells in the experimental group and the control group was 21.6%±2.4% and 62.7%±4.1%, respectively. The proliferation ability of HCT116 cells in the experimental group decreased significantly ( P<0.05) . Conclusions:The expression of FAM83A is significantly increased in colorectal cancer tissues, which may be related to the malignant degree of colorectal cancer. FAM83A affects the proliferation of colorectal cancer cells through the P13K/AKT/mTOR signaling pathway.

Objective:To compare the efficacy and safety of a new type of plastic biliary stent modified based on the pigtail nasobiliary duct and the common plastic biliary stent for hilar cholangiocarcinoma.Methods:Data of a total of 38 patients with obstructive jaundice caused by hilar cholangiocarcinoma who received endoscopic retrograde cholangiopancreatography (ERCP) palliative treatment at the Endoscopy Center, General Hospital of Northern Theater Command from June 2018 to December 2020 were collected, including 20 cases using the new type of plastic biliary stent (the new stent group), and 18 cases using the common plastic stent (the common stent group). Patients were followed up to May 30, 2021. The procedure time, hospital stay, postoperative biliary infection incidence, the bilirubin decrease, and the patency time of the stents in the two groups were compared.Results:The procedure time was 19.85±1.07 minutes in the new stent group and 22.00±3.38 minutes in the common stent group, respectively, showing no significant difference between them ( t=1.26, P=0.607). The lengths of hospital stay of the two groups were 11.45±2.39 days and 11.33±3.51 days, respectively, showing no significant difference between them ( t=-0.52, P=0.938). The median margins of total bilirubin reduction in the two groups were 122.85 μmol/L and 96.25 μmol/L, respectively, with significant difference ( Z=-2.03, P=0.042). The incidence of long-term cholangitis of the new stent group was significantly lower than that of the common stent group [10.0% (2/20) VS 44.4% (8/18), P=0.027]. The patency time of the new stent group was significantly longer than that of the common stent group (109.45±32.67 days VS 82.11±20.95 days) with significant difference ( t=2.23, P=0.032). Conclusion:In the palliative treatment of hilar bile duct obstruction, the new plastic bile duct stent modified based on pigtail type can reduce the incidence of long-term cholangitis and prolong the patency of bile duct stent compared with the common stent group.

Tuberculosis (TB) is an ancient infectious disease. Before the availability of effective drug therapy, it had high morbidity and mortality. In the past 100 years, the discovery of revolutionary anti-TB drugs such as streptomycin, isoniazid, pyrazinamide, ethambutol and rifampicin, along with drug combination treatment, has greatly improved TB control globally. As anti-TB drugs were widely used, multidrug-resistant (MDR) and extensively drug-resistant (XDR) strains of Mycobacterium tuberculosis emerged due to acquired genetic mutations, and this now presents a major problem for effective treatment. Genes associated with drug resistance have been identified, including katG mutations in isoniazid resistance, rpoB mutations in rifampin resistance, pncA mutations in pyrazinamide resistance, and gyrA mutations in quinolone resistance. The major mechanisms of drug resistance include loss of enzyme activity in prodrug activation, drug target alteration, overexpression of drug target, and overexpression of the efflux pump. During the disease process, Mycobacterium tuberculosis may reside in different microenvironments where it is expose to acidic pH, low oxygen, reactive oxygen species and anti-TB drugs, which can facilitate the development of non-replicating persisters and promote bacterial survival. The mechanisms of persister formation may include toxin-antitoxin (TA) modules, DNA protection and repair, protein degradation such as trans-translation, efflux, and altered metabolism. In recent years, the use of new anti-TB drugs, repurposed drugs, and their drug combinations has greatly improved treatment outcomes in patients with both drug-susceptible TB and MDR/XDR-TB. The importance of developing more effective drugs targeting persisters of Mycobacterium tuberculosis is emphasized. In addition, host-directed therapeutics using both conventional drugs and herbal medicines for more effective TB treatment should also be explored. In this article, we review historical aspects of the research on anti-TB drugs and discuss the current understanding and treatments of drug resistant and persistent tuberculosis to inform future therapeutic development.
Humans ; Pyrazinamide/therapeutic use* ; Isoniazid/therapeutic use* ; Antitubercular Agents/therapeutic use* ; Tuberculosis, Multidrug-Resistant/microbiology* ; Mycobacterium tuberculosis/genetics* ; Tuberculosis/drug therapy* ; Rifampin/therapeutic use* ; Mutation ; Drug Resistance, Multiple, Bacterial/genetics*