Objective To explore the molecular mechanisms by which cucurbitacin B(CuB)regulates the mitochondrial ap-optosis pathway through the nicotinamide phosphoribosyltransferase(NAMPT)/forkhead transcription factor O subfamily member 3a(FoxO3a)axis to affect the biological function of non-small cell lung cancer(NSCLC)cells.Methods Gefitinib(GEF)and CuB were used to intervene in A549 cells.Network pharmacology was employed to analyze the targets and downstream pathways,and different vector-transfected cell groups were set up.Cell viability was detected by CCK-8 assay,cell invasion by Transwell assay,and cell apoptosis by flow cytometry.The mitochondrial membrane potential(MMP)level was measured using a JC-1 kit,and intracellular reactive oxygen species(ROS)levels were detected using a kit.Western blot was used to detect the expression of mitochondrial dynamics-related proteins(DRP1,Mfn1),as well as the protein levels of NAMPT and FoxO3a in A549 cells.The mRNA expression of NAMPT was detected by qRT-PCR.Additionally,a xenograft model in nude mice was es-tablished to verify the therapeutic effects of CuB in vivo.Results Compared with the control group,GEF and CuB intervention significantly inhibited the viability and invasion of A549 cells and induced cell apoptosis.Moreover,CuB intervention significant-ly decreased the MMP level,increased ROS concentration,and upregulated the expression of DRP1 while downregulating Mfn1 in A549 cells(P＜0.05).NAMPT,a therapeutic target,was highly expressed in A549 cells and was inhibited by CuB.Compared with the vector group,overexpression of NAMPT significantly promoted the growth of A549 cells and inhibited mitochondrial apoptosis.Compared with the vector+CuB(100 nmol/L)group,overexpression of NAMPT reversed the effects of CuB on A549 cells(P＜0.05).Compared with the si-NAMPT-NC group,silencing NAMPT significantly inhibited the growth of A549 cells and promoted mitochondrial apoptosis,while knockdown of FoxO3a enhanced the viability and invasion of A549 cells and re-versed the damaging effects of si-NAMPT on cancer cells(P＜0.05).In vivo experimental results showed that CuB inhibited tumor weight and volume in a dose-dependent manner.Conclusion CuB regulates the NAMPT-FoxO3a axis through the mito-chondrial apoptosis pathway to inhibit the progression of NSCLC both in vitro and in vivo.

Objective To explore the molecular mechanisms by which cucurbitacin B(CuB)regulates the mitochondrial ap-optosis pathway through the nicotinamide phosphoribosyltransferase(NAMPT)/forkhead transcription factor O subfamily member 3a(FoxO3a)axis to affect the biological function of non-small cell lung cancer(NSCLC)cells.Methods Gefitinib(GEF)and CuB were used to intervene in A549 cells.Network pharmacology was employed to analyze the targets and downstream pathways,and different vector-transfected cell groups were set up.Cell viability was detected by CCK-8 assay,cell invasion by Transwell assay,and cell apoptosis by flow cytometry.The mitochondrial membrane potential(MMP)level was measured using a JC-1 kit,and intracellular reactive oxygen species(ROS)levels were detected using a kit.Western blot was used to detect the expression of mitochondrial dynamics-related proteins(DRP1,Mfn1),as well as the protein levels of NAMPT and FoxO3a in A549 cells.The mRNA expression of NAMPT was detected by qRT-PCR.Additionally,a xenograft model in nude mice was es-tablished to verify the therapeutic effects of CuB in vivo.Results Compared with the control group,GEF and CuB intervention significantly inhibited the viability and invasion of A549 cells and induced cell apoptosis.Moreover,CuB intervention significant-ly decreased the MMP level,increased ROS concentration,and upregulated the expression of DRP1 while downregulating Mfn1 in A549 cells(P＜0.05).NAMPT,a therapeutic target,was highly expressed in A549 cells and was inhibited by CuB.Compared with the vector group,overexpression of NAMPT significantly promoted the growth of A549 cells and inhibited mitochondrial apoptosis.Compared with the vector+CuB(100 nmol/L)group,overexpression of NAMPT reversed the effects of CuB on A549 cells(P＜0.05).Compared with the si-NAMPT-NC group,silencing NAMPT significantly inhibited the growth of A549 cells and promoted mitochondrial apoptosis,while knockdown of FoxO3a enhanced the viability and invasion of A549 cells and re-versed the damaging effects of si-NAMPT on cancer cells(P＜0.05).In vivo experimental results showed that CuB inhibited tumor weight and volume in a dose-dependent manner.Conclusion CuB regulates the NAMPT-FoxO3a axis through the mito-chondrial apoptosis pathway to inhibit the progression of NSCLC both in vitro and in vivo.

OBJECTIVE To investigate the improvement effects and potential mechanism of ulinastatin(UTI)on cisplatin(CP)-induced myocardial injury.METHODS Rabbits were used as study subjects and randomly divided into blank group(normal saline 2 mL/d,for consecutive 7 d),CP group(150 mg/m2,on the 1st and 4th day),UTI low-dose/high-dose group(UTIL/UTIH group,UTL 25 000 or 50 000 IU/kg,once a day,for consecutive 7 d),c-Jun N-terminal kinase(JNK)inhibitor group(JNKi group,SP600125 15 mg/kg,on the 1st and 4th day+CP 150 mg/m2,on the 1st and 4th day+normal saline 2 mL/d,on the other 5 days).Except for the blank group,rabbits in the other groups were injected with relevant medicine and/or normal saline via a marginal ear vein on one side.The serum level of cardiac troponin Ⅰ(cTnⅠ)in rabbits on the 1st and 8th days of the detection experiment,as well as the levels of superoxide dismutase(SOD),glutathione(GSH)and malondialdehyde(MDA)in myocardial tissue on the 8th day of the experiment,were all measured in each group.The pathological changes and myocardial cell apoptosis in myocardial tissue were observed,and the protein expressions of B-cell lymphoma-2(Bcl-2),Bcl-2 associated X protein(Bax),JNK,phosphorylated JNK(P-JNK),mitochondrial fission factor(Mff),and dynamin-related protein 1(Drp1)in myocardial tissue were all determined.RESULTS Compared with the blank group,the CP group showed significant myocardial injury.The cell apoptotic rate,the levels of cTnⅠ in serum and MDA in myocardial tissue,as well as protein expressions of Bax,JNK,p-JNK,Mff,and Drp1,were all significantly increased or up-regulated,SOD level and protein expression of Bcl-2 significantly reduced or down+regulated(P＜0.05).Compared with the CP group,the myocardial injury in rabbits from each drug treatment group showed improvement.The cell apoptosis index,the levels of cTnⅠ in serum and MDA in myocardial tissue,as well as protein expressions of Bax,JNK,p-JNK,Mff(except for UTIL group),and Drp1,were all significantly reduced or down-regulated,while SOD,GSH level and protein expression of Bcl-2 significantly increased or up-regulated(P＜0.05);moreover,the improvement in some indicators was significantly better in the UTIH group and the JNKi group compared to the UTIL group(P＜0.05).CONCLUSIONS UTI may ameliorate CP-induced myocardial injury,the potential mechanism of which may be associated with antagonizing oxidative stress and inhibiting the JNK/Mff signaling pathway.

Objective: Intraperitoneal chemotherapy is increasingly being used in the treatment of gastric cancer with peritoneal me-tastasis, because the drug can directly act on the metastatic nodules. Repeated treatment can be administered through implanted ports, provided the ports are appropriately managed. Our study aimed to investigate the safety of peritoneal port implantation in pa-tients with gastric cancer with peritoneal metastasis. Methods: We retrospectively reviewed the records of patients undergoing intra-peritoneal port implantation for the administration of chemotherapy between June 2015 and June 2018 to investigate the causes of complications and to discuss their management and prevention. Results: Fifty-five ports were implanted in 54 patients with median us-age time of 8.4 (0.8-32.0) months. Complications occurred at 13 port sites (23.6%), including obstruction (7.3%), severe pain (5.5%), in-fection (3.6%), reflux (3.6%), access difficulty (1.8%), and subcutaneous mass formation (1.8%). The median interval from the time of port implantation to the development of complications was 2.1 months. No factor contributing to the complications was identified (P>0.05). Conclusions: Peritoneal port implantation to systematic chemotherapy in patients with gastric cancer with peritoneal metastasis is safe and feasible if the ports can be carefully managed.

Objective To validate the determination method of microbacteria limit of Shuitiaosan powder .Methods Plate counting method was used .The method of counting bacteria and mould was validated by the recovery rates with 5 control strains .The method of checking control bacteria was validated by observing cultivation of Staphylococcus aureus and Pseudomonas aeruginosa in the test group, positive control group and negative control group in the same environment .Results The recovery rate of every trail strains was higher than 70%when centrifugal sedimentation methods were used in the counting bacteria and mould .To the examination of con-trol bacteria , Staphylococcus aureus and Pseudomonas aeruginosa were detected by the centrifugal sedimentation methods .The tested strains were observed in the test group and in the positive control group .No strains were observed in the negative control group .Con-clusion The methods are simple , feasible, reliable and can be used for the examination of microbacteria limit .