OBJECTIVE To explore the mechanism of action of active components of Nostoc commune in anti-triple-negative breast cancer(TNBC) by the network pharmacology method and molecular biology experiment. METHODS The active components of Nostoc commune were collected by consulting the literature and combined with the preliminary research in the laboratory, the Swiss Target Prediction database was used for target prediction, and the disease targets were obtained in the TTD, Genecards and OMIM databases. The STRING online platform was used for protein-protein interaction, and the KEGG signaling pathway and GO gene function enrichment analysis were performed using the Metascape database. Molecular docking of N-acetyltryptamine, a component of Nostoc commune, and target AKT1 by AutoDock software. Annexin V-FITC/PI double staining method was performed to analyze the apoptotic rate of cells. RT-qPCR and Western blotting were used to detect the mechanism of action of the active components of Nostoc commune on anti-TNBC. RESULTS The results of network pharmacology showed that there were 8 effective components, such as N-acetyltryptamine, Scytonemin and Nostocionone, involved 75 key targets such as signal transduction and AKT1, STAT3 and CCND1. The KEGG signaling pathway and GO gene function enrichment analysis results involved cancer-related signaling pathways, PI3K-Akt signaling pathways and MAPK signaling pathways. Molecular docking showed that N-acetyltryptamine had better affinity with AKT1. N-acetyltryptamine could not significantly promote apoptosis of breast cancer cells. Western blotting showed that N-acetyltryptamine could down-regulate the protein expressions of AKT1. The results of RT-qPCR showed that N-acetyltryptamine could effectively reduce the mRNA expression of AKT1 in cells. CONCLUSION N-acetyltryptamine may inhibit the proliferation of TNBC cells by inhibiting the AKT1 signaling pathway, thereby exerting anti-TNBC effects.

Aim To investigate whether DCP has pro- teetive effeet on 2 ,4-dimethylnitrosamine ( DMN) -induced liver fibrosis rat model and its effect on MAPK signaling pathway.Methods Hats were intraperitoneal ly injected with DMN to establish HF model,and then were randomly divided into five groups, namely model group, colchicine group, DCP low-dose, medium-dose and high-dose groups,and control group.The rats were given DMN continuously for six weeks.Serum was col-lected afterwards to detect biochemical indexes of liver function.HE and Masson staining and immunohisto- chemical experiments were performed on liver tissues.RT-PCR was applied to detect the expression of inflammatory factors.Western blot was used to detect the ex pression of proteins related to MAPK pathway,the preventive effect of DCP on HF was observed, and its in-tervention effect on MAPK pathway was explored.Results The liver function of rats in model group was severely impaired, with obvious hepatocyte damage, inflammatory cell infiltration and increased interstitial fibrosis , suggesting that the preparation of HF model was successful.Conclusions DCP can interfere with MAPK signaling pathway to inhibit the inflammatory response and alleviate the progression of HF in rats.

OBJECTIVE To investigate the therapeutic effect of natural phenolic compound p-hydroxybenzoic acid(HA) on adjuvant arthritis(AA) induced by the complete Freund's adjuvant(CFA), and to clarify the mechanism of HA preliminary. METHODS Apart from the normal group, all rats received 0.1 mL CFA by plantar subcutaneous injection to induce AA rats model. And rats with AA were randomized to the model group, the low-, medium-, and high-dose HA group(2.5, 5, and 10 mg·kg-1, respectively), the positive control group(indomethacine, 5 mg·kg-1). The rats in each group were orally treated with the corresponding drugs for therapeutic intervention. The volume and leg thickness of the rats in each group were recorded and an inflated articular score was obtained. Inflammation cytokine expression(TNF-α, IL-1β and IL-6) was determined by ELISA and qPCR. Radiographs and HE staining were used to observe histopathological and pathological changes in the foot. The expressions of caspase-1 and NF-κB were examined in Western blotting. RESULTS HA could significantly alleviate joint swelling in AA rat(P<0.05), inhibited the production of inflammatory factors(TNF-α, IL-1β and IL-6) from protein and mRNA levels(P<0.05), and decreased the expression levels of caspase-1 and NF-κB at protein level(P<0.05). HA alleviated ankle injury in rats by X-ray examination, and HE staining showed that HA could significantly inhibit the infiltration of inflammatory cells and the destruction of cartilage surface(P<0.05), and these results were dose-dependent. CONCLUSION HA may relieve rheumatoid arthritis by inhibiting the NF-κB/casepase-1 signaling pathway.

Aim To investigate the protective effect of mogroside V on hydrogen peroxide ( H,02 )-induced oxidative stress response in mouse islet (3 cells MIN6 and the relation of its mechanism to PI3K/Akt signa¬ling pathway.Methods MIN6 cells were treated with 500 (jimol • L_1 H,(), after mogroside V,and cell via¬bility was detected by MTT.The release of reactive ox¬ygen species ( ROS) and apoptotic percentage of MIN6 cells were determined by flow cytometry.The expres¬sions of apoptosis-related factor Bel-2 , proliferation-re¬lated factor PCNA, protein Akt and p-Akt were deter¬mined by Western blot.Results H,02 restrained the proliferation of MIN6 cells obviously, induced ROS pro¬duction and apoptosis, and reduced the expression of Bel-2 and PCN A.The expressions of protein Akt and p-Akt decreased.After treatment of mogroside V , the release of ROS decreased, and the apoptosis of MIN6 cells was inhibited.The expression levels of apoptosis- related protein Bcl-2 and proliferation-related protein PCN A were reversed.The expressions of protein Akt and P-Akt increased.The viability of MIN6 cells in¬duced by H,0, increased.In addition, mogroside V partly reversed the apoptosis induction and ROS pro¬duction of Akt inhibitor MK2206 (5 jjimol • L"1 ) on MIN6 cells.Conclusions Mogroside V has protec¬tive effect on H202-induced oxidative damage in MIN6 cells and its mechanism is related to PI3K/Akt signa¬ling pathway.

Objective: To explore effectiveness of Tai Ji exercise on the shoulder, neck and back pain caused by sedentary lifestyle among college students. Methods: Totally 350 college students with shoulder, neck or back pain were divided into two groups by random number table method (n=175). The control group received no exercise prescription intervention, while the intervention group received Taijiquan exercise for 12 weeks. The changes of cervical Japanese Orthopaedic Association (JOA) score, lumbar JOA score and VAS score before and after intervention were compared between the two groups. Results: The scores of upper limb motor function, lower limb motor function, sensory function, subjective symptoms, clinical signs and daily activity limitation in the intervention group were significantly higher than those in the control group (P<0.05). The VAS score of the intervention group after intervention was (1.51±0.63), which was significantly lower than that of the control group (3.49±0.75, P<0.05). The improvement in frequency and duration of pain in the intervention group were more significant than those in the control group(P<0.05). The rate of symptom improvement was significantly higher in the intervention (86.86%), than that of the control group (4.00%, P<0.05). Conclusion For the shoulder, neck and back pain caused by sedentary lifestyle, the practice of Tai Ji exercise can effectively relax the muscles and the joint tissue. The results show effectiveness in alleviating shoulder, neck and back pain among college students.

OBJECTIVE： To study the in vitro inhibitory effects and antioxidant activity of different solvent extracts of Boehmeria nivea leaves against influenza A virus（H1N1）， and to expand the medicinal parts of B. nivea and develop natural antiviral and antioxidant drugs. METHODS： The leaves of B. nivea were extracted with 95％ ethanol. The ethanol extract was dissolved by water heating， and extracted with different solvents to obtain petroleum ether phase， trichloromethane phase， ethyl acetate phase， n-butanol phase and aqueous phase extracts of B. nivea leaves. The toxicity of aqueous extract of B. nivea leaves （50-400 μg/mL） on Madin-Darby canine kidney （MDCK） cell line was investigated. Using ribavirin as positive control， MDCK cells were attacked by influenza A virus（H1N1）. Western blotting assay was used to detect the expression of nucleoproteins （NP） in viral infected cells after treated with same concentrations of petroleum ether phase， trichloromethane phase， ethyl acetate phase， n-butanol phase and aqueous phase extracts of B. nivea leaves （100 μg/mL）， different concentrations of aqueous phase extract solution of B. nivea leaves （50， 100， 200， 400 μg/mL） and different concentrations of ribavirin solution （0.31， 0.63， 1.25 μg/mL）. Using vitamin C as a positive control， hydroxyl radical（·OH） scavenging test， DPPH radical scavenging test and reduction test were used to investigate in vitro antioxidant activity of the extracts. RESULTS： Aqueous phase extract of B. nivea leaves with concentration less than 400 μg/mL was nontoxic to MDCK cells. The petroleum ether phase， trichloromethane phase， ethyl acetate phase and aqueous phase extracts at 100 g/mL could significantly reduce the expression of NP protein in influenza A virus（H1N1） infected cells （P＜0.01）. Different concentrations （50-400 μg/mL） of aqueous extract could significantly reduce the protein expression of NP （P＜0.01） in concentration-dependent manner. The in vitro antioxidant activity of petroleum ether phase and ethyl acetate phase was similar to that of vitamin C. CONCLUSIONS： B. nivea leaves extract have better anti-influenza A virus（H1N1） effects in vitro， and the extracts of petroleum ether phase and ethyl acetate phase show good antioxidant activity in vitro.

Aim To investigate the potential mechanism of osthole promoting autophagy in cervical cancer HeLa cells. Methods HeLa cells were treated with various concentrations of Osthole(0,10,20,40,80,160,240,320 mg·L-1). MTT was used to detect cell vitality. Transmission electron microscopy(TEM)was used to observe the morphology of HeLa cells after osthole intervention. Mondane sulfonyl cadaverine(MDC)staining was used to dectect the level of autophagy. Western blot was employed to analyze the expression levels of mitochondrial protein MFN1 and DPR1. JC-1 flourescence probe was applied to detect mitochondrial membrane potential. Flow cytometry was used to deteminet the release of reactive oxygen species(ROS). A transplanted tumor model of cervical cancer was established in vivo in nude mice. Western blot was used to detect the protein expression levels of PINK1,Parkin and LC3Ⅱ/. Results Osthole could inhibit the proliferation of HeLa cells significantly. Transmission electron microscopy showed that typical autophagosomes were formed in HeLa cells after osthole intervention. The fluorescence intensity of MDC was enhanced. The expression of mitochondrial fusion protein MFN1 was down-regulated after HeLa cells pretreated with osthole,and mitochondrial fission protein DRP1 was up-regulated. Mitochondrial membrane potential decreased. ROS production of HeLa cells was increased by flow cytometry,which could be reversed by autophagy inhibitor 3-MA. Tumor weight in nude mice was inhibited by osthole obviously,which might restrain cervical cancer. Western blot result indicated that the key factors of mitochondrial autophagy PINK1,Parkin and LC3Ⅱ/ratio were up-regulated in HeLa cells. Conclusions Osthole could induce autophagy in HeLa cells and its mechanism may be related to ROS production and PINK1/Parkin pathway.

OBJECTIVE To study the mechanism of curcumol inhibiting the pro liferation of breast cancer cells T 47D. METHODS MTT assay was used to detect the inhibitory effects of different doses of curcumol （0，6.25，12.5，25，50，100 μg/mL）on the proliferation of T 47D cells. After treated with curcumol （12.5，25，50，100 μg/mL），the morphology of T 47D cells was observed by inverted phase contrast microscope. The cell cycle and the levels of reactive oxygen species （ROS）were detected by flow cytometry. Quantitative real-time PCR （qRT-PCR）was used to detect the expressions of proliferating cell nuclear antigen （PCNA），cell cycle regular p 21 and cyclin-dependent kinase 2（CDK2）mRNA. Western blot assay was used to detect the protein expression of CDK 2，CDK6，Cyclin D ，PCNA，nucler transcription factor E 2-related factor （Nrf2）and Kelch-like ECH associated protein 1（Keap1）. Breast cancer cells T 47D were divided into 2 groups，one group was given different doses of curcumol ，and another group was given curcumol 33 μg/mL for 6，12，24，48 h. After the optimal oxidation time and administration concentration were determined according to the results of the above two groups ，the blank control group ，N-acetylcysteine（NAC）group（ROS antioxidant NAC alone ），curcumol group （curcumol alone ），curcumol combined with NAC group （pretreatment with ROS antioxidant NAC ，and then adding into curcumol ）. Cell cycle and fluorescence intensity of ROS were detected. RESULTS Curcumol could significantly increase the inhibitory rate of the proliferation of T 47D cells （P＜0.05 or P＜0.01），and showed a certain dose and time dependent trend. Curcumol blocked the ， cycle in the G 1 phase and significantly increased the level of ROS （P＜0.05 or P＜0.01）；ROS antioxidant NAC could significantly reverse above inductive effect of curcumol （P＜ 0.01）. qRT-PCR showed that curcumol down-regulated the com expression of PCNA and CDK 2 mRNA and up-regulated the expression of p 21 mRNA（P＜0.05 or P＜0.01）. Western blot assay showed that curcumol significantly down-regulated the edu.cn protein expression of Keap 1，Nrf2，CDK2，CDK6 and Cyclin D（P＜0.05，P＜0.01）；ROS antioxidant NAC could reverse the down-regulation effects of curcumol on the expression of these proteins（P＜0.05 or P＜0.01）. CONCLUSIONS Curcumol may induce oxidative stress and cell arrest in G 1 phase to inhibit the proliferation of T 47D cells.

OBJECTIVE:To compare the clinical efficacy and safety of Kangshuling gel,mupirocin and lactate ethacridine in the treatment of diabetic foot. METHODS:90 patients with diabetic foot were randomly divided into Kangshuling group,mupiro-cin group and lactate ethacridine group. All the patients were treated by lowing blood glucose,nutritional support,improving micro-circulation and anti-infection,etc. On this basis,3 groups were given Kangshuling gel,Mupirocin ointment and Lactate ethacridine solution for wet compress by gauze. The course was 180 d. The clinic data was observed,including clinical efficacy,and wound ar-ea,healed patients’granulation,epithelial tissue,healing time and incidence of adverse reactions before and after treatment. RE-SULTS:The total effective rate in Kangshuling group was significantly higher than mupirocin group and lactate ethacridine group;healed patients’granulation,epithelial tissue and healing time were significantly shorter than mupirocin group and lactate ethacri-dine group,with significant differences(P<0.05). After treatment,wound area in each group were significantly smaller than be-fore,and Kangshuling group was smaller than mupirocin group and lactate ethacridine group,with significant differences(P<0.05);there were no significant differences between mupirocin group and lactate ethacridine group(P>0.05). There were no obvi-ous adverse reactions during treatment. CONCLUSIONS:Based on the conventional treatment,Kangshuling gel has better efficacy than mupirocin and lactate ethacridine in the treatment of diabetic foot,with good safety.

OBJECTIVE:To explore the clinical features and regularity of drug-induced liver injury (DILI),and to provide reference for clinical rational drug use. METHODS:104 DILI cases in our hospital from 2005 to 2014 were selected and analyzed retrospectively in respects of patient’s gender,age,allergic history,medication history,drug type and clinical manifestations. RE-SULTS:DILI hospitalized cases increased year by year. There were 47 males and 57 females,and average age was(8.71±13.90). The clinical symptoms appeared within 12 weeks after using the drug. The symptoms were no specific,including weak,anorexia, jaundice,yellow urine,etc. and 10.57% of patients were asymptomatic. Most of the DILI cases were hepatocyte type(80.77%), followed by cholestasis type(12.50%)and hybrid type(6.73%). The most common cause of drug-induced liver injury were TCM, antimicrobial drugs and the nervous system drugs. CONCLUSIONS:The incidence of DILI in females is slightly higher than males. DILI often occurs after 40 years old. The clinical symptoms have no specificity and are similar to viral hepatitis. The hepatic lesions can be caused by most of drugs. DILI by TCM should concerned. Clinical physicians should pay more attention to DILI.