Aim To investigate the role of PPARβ and nitrative stress in human umbilical vein endothelial cells(HUVECs)injury induced by high glucose.Methods The cell viability was detected by CCK-8.The cell proliferation was detected by EdU proliferation detection kit.The protein expression level of PPARβ,eNOS,iNOS,and 3-nitrotyrosine was detected by Western blot.The content of peroxynitrite and nitric oxide(NO)was determined by peroxynitrite kit and Griess Reagent,respectively.Results Glucose(30,40,50 mmol·L-1)significantly reduced the cell viability of HUVECs in a dose-dependent manner.Glucose at 30 mmol·L-1(high glucose,HG)significantly reduced the proliferation of HUVECs,down-regulated the expression of PPARβ,eNOS at protein level and NO content,and increased iNOS,3-nitrotyrosine protein expression and peroxynitrite level.The above effects of HG were reversed by PPARβ agonist GW0742(1 μmol·L-1).Both PPARβ antagonist GSK0660(1 μmol·L-1)and NOS inhibitor L-NAME(10 μmol·L-1)blocked the protective effects of GW0742.Conclusion The down-regulation of PPARβ is involved in the injury of HUVECs induced by high glucose,which may be mediated,at least partly,by the stimulation of nitrative stress.

In recent years， the incidence rate of andrological diseases has shown a significant growth trend. Considering the unavailability of a perfect theoretical system for andrology in traditional Chinese medicine （TCM） and the complex pathogenesis despite of the limited types of andrological diseases， it is necessary to improve the clinical efficacy of andrological diseases so as to satisfy the needs of patients. Therefore， the China Association of Chinese Medicine （CACM） organized the andrologists of TCM and western medicine and the outstanding young clinicians to discuss the andrological diseases responding specifically to TCM or integrated TCM and western medicine， such as chronic prostatitis， male infertility， benign prostatic hyperplasia， erectile dysfunction， and premature ejaculation， determine their diagnostic criteria in western medicine， and standardize the specifications for TCM diagnosis and treatment based on syndrome differentiation， thus formulating recognized and integrated diagnosis and treatment protocols. Apart from proposing suggestions on the treatment of such andrological diseases with TCM and western medicine， the experts have also figured out the andrological diseases responding specifically to TCM， the optimal intervention time of TCM and western medicine， and the suitable measures including surgery. The resulting consensus helps to better guide the formulation of accurate， personalized， and optimized treatment plans in clinical practice and improve the diagnosis and treatment effects of andrological diseases by giving full play to the advantages of TCM， which will in turn contribute to further innovation and development of TCM.

Chronic obstructive pulmonary disease (COPD) is a common respiratory disease with a high morbidity, disability and mortality. At the same time, COPD is always accompanied by pulmonary hypertension, pulmonary fibrosis, chronic pulmonary heart disease, right heart failure and other common serious complications. All of these cause serious financial burden for the family of patients. Airway remodeling plays an important role in the pathogenesis of COPD. It is the progressive development of airflow restriction that induces the main symptoms of COPD, such as cough, asthma and depression. Therefore, it is of great research value to explore the intervention of traditional Chinese medicine(TCM) in the development of COPD by alleviating airway remodeling. Studies have shown that multiple signaling pathways can induce progressive airway remodeling, and the therapeutic effect of TCM has been frequently confirmed by experimental studies. TCM often has a therapeutic effect on COPD through multi-target and multi-channel mediation. This paper mainly includes five signaling pathways that traditional Chinese medicine can intervene COPD airway remodeling, namely matrix metalloproteinases (MMPs)/tissue inhibitors of metalloproteinase (TIMPs), transforming growth factor (TGF)-beta 1/Smads, RhoA/Rho-associated kinase (ROCK), vascular endothelial growth factor (VEGF)/b-fibroblast growth factor (b-FGF) and nuclear factor (NF)-κB. This paper briefly reviews the research progress of these five signaling pathways, and discusses other signaling pathways that may be involved, in order to provide reference and ideas for future experimental research.

Objective: To observe the effect of modified Erchentang on GATA-binding protein-3(GATA3) and T-box expressed in T cells(T-bet) in lung tissue of rats with chronic obstructive pulmonary disease (COPD). Method: Seventy SD rats were randomly divided into seven groups, namely normal group, model group, low, medium and high-dose modified Erchentang group(5,10,20 g ·kg^-1), Xiaokechuan group(5 g ·kg^-1) and Erchentang group(5 g ·kg^-1), with 10 in each group. The rat model of COPD was established by smoking combined with intratracheal dripping of lipopolysaccharide (LPS). After successful modeling, the treatment group was given intragastric administration, and the normal group and the model group were given intragastric administration of equal volume of saline. Enzyme-linked immunosorbent assay (ELISA) was used to determine the concentrations of interleukin-10 (IL-10) and interleukin-12 (IL-12) in rat serum. The expressions of GATA3 and T-bet were detected by real-time fluorescence quantitative polymerase chain reaction (Real-time PCR). The expressions of GATA3 and T-bet in lung tissue were detected by immunohistochemistry (IHC). Result: Compared with the control group, the serum levels of IL-10 in the model group was significantly decreased, while the IL-12 level was significantly increased (P<0.01). The protein and gene expressions of GATA3 in lung tissue were significantly decreased, whereas the expression of T-bet was significantly increased (P<0.01). Compared with the model group, the serum level of IL-10 in each treatment group was increased to varying degrees, while the level of IL-12 was decreased to varying degrees (P<0.05). The mRNA and protein expressions of GATA3 in lung tissue of rats in each treatment group were increased significantly, while T-bet was inhibited (P<0.05). Conclusion: Modified Erchentang may reduce the inflammation of lung tissue and improve lung function in COPD rats by reducing IL-12, increasing the content of IL-10, inhibiting the protein and gene expressions of T-bet, and stimulating the protein and gene expressions of GATA3.

Objective: To explore the effect of modified Erchentang on peroxisome proliferator-activated receptor gamma (PPARγ) protein and gene expressions in lung tissue of chronic obstructive pulmonary disease (COPD) rat model, and the expressions of interleukin-6 (IL-6), interleukin-10 (IL-10) and tumor necrosis factor-alpha (TNF-α) in serum, lung homogenate and bronchoalveolar lavage fluid. Method: Seventy SD rats were randomly divided into seven groups:normal group, model group, high, medium and low-dose modified Erchentang groups (40, 20, 10 g · kg^-1 · d^-1), Xiaokechuan group (5 g · kg^-1 · d^-1), and Erchentang group (5 g · kg^-1 · d^-1). The rat COPD model was established through smoking and intratracheal instillation of lipopolysaccharide (LPS). After successful modeling, the treatment group was given drug by gavage, while the normal group and the model group were given the same amount of saline. The concentrations of IL-6, IL-10 and TNF-α in serum, lung homogenate and bronchoalveolar lavage fluid(BALF) of rats were measured by enzyme-linked immunosorbent assay (ELISA). Real-time fluorescence quantitative PCR (Real-time PCR) was used to detect the expression of peroxisome proliferator-activated receptor gamma (PPARγ), and immunohistochemistry (IHC) and Western blot were used to detect the expression of PPARγ in lung tissue. Result: Compared with the normal group, the levels of IL-6 and TNF-α in serum, lung homogenate and BALF of the model group rats increased significantly (P<0.01), while IL-10 decreased significantly (P<0.01). The expressions of PPARγ mRNA in lung tissue of rats in model group were significantly decreased (P<0.01), and the expression of PPARγ protein was significantly inhibited(P<0.01). Compared with the model group, the levels of IL-6 and TNF-α in serum, lung homogenate and BALF of each treatment group decreased to varying degrees(P<0.01), while IL-10 increased to varying degrees. The excitation of IL-10 and the inhibition of IL-6 and TNF-α in the middle-dose Erchentang group were particularly significant. The PPARγ mRNA and protein expressions in lung tissue of rats in each treatment group were increased to varying degrees (P<0.01). Conclusion: Modified Erchentang may improve pulmonary inflammation and pulmonary function in COPD rats by increasing the expression of PPARγ and the content of IL-10 and decreasing the contents of IL-6 and TNF-α.

Objective: To explore the effect of modified Erchentang on the signal pathway of β₂ adrenergicreceptor(β₂AR)/arrestin beta 2(β-arrestin2) in rats with chronic obstructive pulmonary disease (COPD), and the expression of interleukin-17(IL-17) in serum, lung homogenate and bronchoalveolar lavage fluid. Method: Seventy SD rats were randomly divided into seven groups:normal group, model group, modified Erchentang with high, medium and low doses (40, 20, 10 g · kg^-1 · d^-1), Xiaokechuan group (5 g · kg^-1 · d^-1), modified Erchentang group (5 g · kg^-1 · d^-1), 10 rats in each group. The rat model of COPD was established by smoking and lipopolysaccharide (LPS) intratracheal drip. After successful modeling, the treatment group was given intragastric administration, while the normal group and the model group were given the same amount of saline. Enzyme-linked immunosorbent assay (ELISA) was used to detect the levels of IL-17 in serum, lung homogenate and bronchoalveolar lavage fluid of rats. Real-time fluorescence quantitative PCR (Real-time PCR) was used to detect the expression of β₂AR gene. Western blot was used to detect the expression of β₂AR protein in lung tissue. The expression of β₂AR and β-arrestin2 in lung tissue was detected by immunohistochemistry. Result: Compared with the normal group, the expression of β₂AR protein in lung tissue of model group was significantly decreased(P<0.01). Compared with model group, the expression of β₂AR protein in lung tissue was significantly increased(P<0.01), and the middle dose group of modified Erchentang was different from other groups (P<0.05). Compared with normal group, the expression of β₂AR in model group was significantly lower(P<0.01), compared with model group, the expression of β₂AR in high, medium and low dose group, Xiaokechuan group and modified Erchentang group was significantly higher(P<0.01). The middle dosage group of modified Erchentang was significantly higher than other groups(P<0.01). Compared with normal group, the serum level of IL-17 in the model group was significantly higher(P<0.01). Compared with model group, the serum level of IL-17 in each group was inhibited to a certain extent, especially in the middle dose group of modified Erchentang (P<0.05). Conclusion: Modified Erchentang may increase the expression of β₂AR and β-arrestin2 and decrease the content of IL-17 in order to resist inflammation and improve pulmonary function in COPD rats.

Objective: To observe the effects of Erchen on vascular endothelial growth factor (VEGF) and its receptor R2 (VEGFR2), interleukin (IL)-4 and endothelin-1 (ET-1) in rats with chronic obstructive pulmonary disease (COPD). Method: The 50 SD rats were randomly divided into 5 groups, 10 rats in each group, which were normal group, model group, Erchentang low, medium and high dose group (10, 20, 40 g · kg^-1 · d^-1). COPD rat model was established by smoking combined with lipopolysaccharide (LPS) intratracheal drip. After successful modeling, the treatment group was given intragastric administration, and the normal group and the model group were given intragastric distilled water of equal volume. The pathological changes of pulmonary vessels in rats were observed by light microscopy, and the thickness of pulmonary vascular wall was measured. The concentration of IL-4 in rat serum, bronchoalveolar lavage fluid (BALF) and lung homogenate was measured by enzyme-linked immunosorbent assay (ELISA). Real-time fluorescence quantitative polymerase chain reaction (Real-time PCR) was used to detect the expression of ET-1 and immunohistochemistry was used to detect the expression of VEGF,VEGFR2 and ET-1 in lung tissue. Result: Compared with normal group, the concentration of IL-4 in serum, BALF and lung homogenate of model group rats decreased significantly (P<0.05).Compared with model group, the concentration of IL-4 in low, medium and high dose Erchentang group increased in varying degrees (P<0.05). Compared with normal group, the expression of ET-1 in lung tissue of model group was significantly increased (P<0.05).C ompared with model group, the expression of ET-1 in lung tissue of low, medium and high dose Erchentang group was significantly decreased (P<0.05). Compared with normal group, the expression of VEGF, VEGFR2, ET-1 protein in the lung tissue of model group increased (P<0.05). Compared with model group, the expression of VEGF, VEGFR2 and ET-1 protein in the low, medium and high dose Erchentang group decreased (P<0.05). Conclusion: Modified Erchentang can alleviate the process of pulmonary inflammation and pulmonary vascular remodeling in COPD rats, and slow down the progress of COPD and its complications by increasing the content of IL-4, inhibiting the expression of VEGF, VEGFR2, ET-1.

Five secondary metabolites, including a new isopimarane derivative xylaroisopimaranin A (1), were isolated from the endophytic fungus Xylaralyce sp. (HM-1), and their structures were elucidated by 1D, 2D NMR, MS and CD spectra. Their bioactivities were performed to antibacterial, Hep G2 cells cytotoxicity and brine shrimp inhibition. The biological evaluation results showed that the xylaroisopimaranin A (1), xylabisboein B (2), griseofulvin (3) , 5-methylmellein (4) and mellein-5-carboxlic acid (5) displayed no significant Hep G2 cells cytotoxicity and antibacterial acitivity, but they inhibited the brine shrimp with IC₅₀ from 0.5 to 25 µmol/mL.
Artemia ; Fungi ; Griseofulvin ; Hep G2 Cells

OBJECTIVETo investigate the efficacy and possible action mechanism of Qianlie Beixi Capsule in the treatment of unliquefiable semen.

METHODSA total of 240 patients with unliquefiable semen were randomly divided into a treatment group (n = 180), treated with Qianlie Beixi Capsule, and a control group (n = 60), given compound tablets of zinc and protein. The treatment lasted two courses of 45 days each, and the seminal changes were observed and recorded.

RESULTSOf the patients in the treatment group, 144 were cured, 12 responded and 24 failed to respond to the medication after the first course; and 158 were cured, 7 responded and 15 failed to after the second course, with the effectiveness rate of 91.67%. Meanwhile, sperm motility was obviously improved, with statistically significant difference from that of the controls (P < 0.01).

CONCLUSIONQianlie Beixi Capsule is effective for unliquefiable semen by improving the function of the prostate and shortening the time of seminal liquefaction.

Adult ; Drugs, Chinese Herbal ; therapeutic use ; Humans ; Infertility, Male ; drug therapy ; etiology ; Male ; Middle Aged ; Phytotherapy ; Sperm Motility