Emodin induces apoptosis in human prostate cancer cell LNCaP

Aim： To elucidate effects and mechanisms of emodin in prostate cancer cells. Methods： Viability of emodin-treated LNCaP cells and PC-3 cells was measured by MTT assay. Following emodin treatments, DNA fragmentation was assayed by agarose gel electrophoresis. Apoptosis rate and the expression of Fas and FasL were assayed by flow cytometric analysis. The mRNA expression levels of androgen receptor （AR）, prostate-specific antigen （PSA）, p53, p21, Bcl-2, Bax, caspase-3, -8, -9 and Fas were detected by RT-PCR, and the protein expression levels of AR, p53 and p21 were detected by Western blot analysis. Results： In contrast to PC-3, emodin caused a marked increase in apoptosis and a decrease in cell proliferation in LNCaP cells. The expression of AR and PSA was decreased and the expression of p53 and p21 was increased as the emodin concentrations were increased. In the same time, emodin induced apoptosis of LNCaP cells through the upregulation of caspase-3 and -9, as well as the increase of Bax/Bcl-2 ratio. However, it did not involve modulation of Fas or caspase-8 protein expression. Conclusion： In prostate cancer cell line, LNCaP, emodin inhibites the proliferation by AR and p53-p21 pathways, and induces apoptosis via the mitochondrial pathway.

Dehydrocostus lactone exerts the antitumor effect in non-small cell lung cancer H1299 cells

Background:Dehydrocostus lactone(DHC),a sesquiterpene lactone derived from Aucklandiae Radix,has been proved to possess various pharmacological activities.Recently,studies have reported that DHC has potential antitumor activity.However,few studies have reported the effect of DHC on non-small cell lung cancer(NSCLC).Here,we investigated the antitumor effect of DHC in NSCLC H1299 cells.Methods:MTT assay and colony formation assay was used to assess the anti-proliferation effects of DHC in H1299 cells.Wound healing and Transwell assays were utilized to determine the inhibitory effects of migration and invasion,respectively.Apoptosis was detected using the Annexin V/propidium iodide test.Real-time-quantitative PCR(RT-qPCR)was used to detect the mRNA expression level.Results:We demonstrated here that DHC inhibited the proliferation,migration and invasion of H1299 cells in a dose-or time-dependent manner.Additionally,after treating with DHC at the concentration of 32.0μM,the apoptosis of H1299 cells was significantly induced.Moreover,DHC affected the mRNA expression of E-cadherin,N-cadherin,Snail,c-Myc,integrinα2,Survivin and matrix metalloproteinase 2.Conclusion:To summarize,our data support that DHC can inhibit proliferation,invasion,migration and induced apoptosis of NSCLC H1299 cells.DHC should be considered for its potential for adjuvant therapeutic development.

Brusatol Inhibits Proliferation,Migration,and Invasion of Nonsmall Cell Lung Cancer PC-9 Cells

Objective:The purpose of this study was to investigate the inhibitory effect of brusatol,a nigakilactone extracted from Brucea javanica,on lung cancer for development of therapeutic drugs.We explored the effects of brusatol on the proliferation,migration,and invasion of lung cancer PC-9 cells in vitro and analyzed the mechanisms involved.Materials and Methods:MTT assay was used to determine the effect of brusatol on the proliferative capacity of PC-9 and H1975 cells in vitro.The half-maximal inhibitory concentrations(IC_(50))were calculated and used as a reference for subsequent experiments.Variations in the number and size of tumor cell clusters were monitored by the colony formation assay as evidence for the effect of brusatol on cell proliferation.The effect of brusatol on the migration and invasion of PC-9 cells was evaluated using wound healing and transwell assays,respectively.Apoptosis in lung cancer cells was detected using the Annexin V-FITC/propidium iodide assay.The correlated anticancer mechanism was detected using Western blotting.Results:The IC_(50)values of brusatol acting on PC-9 and H1975 cells were 1.58±0.30μM and 31.34±2.72μM,respectively,according to the MTT experiment.In addition,brusatol suppressed PC-9 cell proliferation,migration,and invasion,as well as induced apoptosis,which may be related to the downregulation of epidermal growth factor receptor(EGFR),β-catenin,Akt,and STAT3 expression.Conclusions:Brusatol showed potent anticancer activity against lung cancer PC-9 cells,inhibiting the proliferative capacity and metastatic potential of PC-9 cells.Its anticancer effect may be related to the downregulation of EGFR,β-catenin,Akt,and STAT3.

Effect of prolactin on penile erection:a cross-sectional study

Although elevated prolactin levels have been shown to inhibit penile erection,the relationship between prolactin and erection of the penile tip or base has not been extensively researched.We therefore investigated the prolactin's effects on erecti on of the penile tip and base,with a cross-secti onal study of 135 patie nts with erectile dysfuncti on,based on scores of M21 on the In ternational Index of Erectile Function-5.All patients were tested for nocturnal penile tumescenee,blood pressure,serum glucose,total cholesterol,triglyceride,high-density lipoprotein,low-density lipoprotein,luteinizing hormone,follicle-stimulating hormone,prolactin,estradiol,testosterone,and progesterone.Univariate and multivariate analyses were used to assess the associations between prolactin levels and erection at the penile tip and base.We found no obvious relati on ship between erection time at penile tip and prolactin levels,but observed a negative correlation between base erection time and prolactin level(hazard ratio:-2.68;95%confidence interval[Cl]:-5.13-0.22).With increasing prolactin concentration,multivariate analysis showed obvious reduction in base erection time among patients with normal Rigiscan results(hazard ratio:-3.10;95%Cl:-7.96-1.77;P<0.05).Our data indicate that prolactin inhibits penile erection,particularly at the penile base.In addition,when the effective erection time of the penile base lasts longer than 10 min,prolactin has a more obvious inhibitory effect on penile base erection.

A Study on the Mechanism of Bruceine D in the Treatment of Non-small Cell Lung Cancer H1299 Cells

Background:Non-small cell lung cancer(NSCLC)is considered one of the leading causes of cancer-related death.Despite the availability of drugs for the treatment of NSCLC,the need for the development of novel agents with high efficiency and fewer adverse effects remains unmet.The natural compound bruceine D(BD)is widely recognized for its notable anti-inflammatory,antiparasitic,and hypoglycemic activities.However,it is unclear whether BD can be used as a novel agent for NSCLC treatment.Materials and Methods:MTT and colony formation assays were used to assess the antiproliferative effect of BD on NSCLC cells.Wound healing and transwell assays were performed to determine the effect of BD on the migration and invasion of H1299 cells,respectively.Western blotting assay was used to detect the expression levels of proteins.Results:We demonstrated that BD significantly inhibited the proliferation of H1299,A549,and H226 cells with respective IC50 values of 6.06±0.52,7.15±0.90,and 7.21±0.75μM.In addition,BD suppressed colony formation of H1299 cells in a dose-dependent manner.Following treatment with BD,the migration and invasive capabilities of H1299 cells were significantly inhibited in a dose-and time-dependent manner.Moreover,the results of Western blotting demonstrated that BD treatment resulted in the upregulation of the protein expression of E-cadherin and downregulation of the expression of N-cadherin,twist,snail,integrinαv,integrinβ4,matrix metalloproteinase-7,andβ-catenin proteins.Conclusion:BD inhibits proliferation,migration,and invasion of NSCLC cells;therefore,BD may be considered for its potential in adjuvant therapy for NSCLC.

Vlean platelet volume might.be an effective ndicator of arterial erectile dysfunction

The aim of our study was to investigate the role of platelet parameters including mean platelet volume (MPV)and platelet count (PC) in the pathogenesis of penile arteriogenic erectile dysfunction (ED)and to evaluate the association between the platelet parameters and arteriogenic ED.There were 244 patients with ED (based on the International Index of Erectile Function [IIEF]-5≤21)and 60 healthy controls (IIEF-5 >21)enrolled.All participants were asked to undergo a laboratory examination,and penile vascular function was evaluated using penile color Doppler ultrasonography (pDUS).Among these ED patients,24 patients with no abnormality on nocturnal penile tumescence (NPT)and 84 with normal vasculature or mixed vascular abnormalities were excluded.The other patients were classified into three groups as follows:control (n =60),arteriogenic ED (n =99),and venous leakage (n =37) groups.MPV and PC were significantly higher in the arteriogenic ED group compared with the venous and control groups (P<0.05). Receiver operating characteristic curve analysis revealed that the area under the curve for MPV to predict arteriogenic ED was 0.707. MPV≥9.65 fl was recognized as a cut-off value for potential arteriogenic ED (sensitivity:47.5%;specificity:91.7%).A significant inverse correlation was detected between MPV and lO-min peak systolic velocity (PSV)(r =-0.34;P <0.001)in the arteriogenic ED group.These findings suggest that the MPV might be a powerful indicator to predict and diagnose arteriogenic ED,and MPV may be a marker for ED when using pDUS.

ANTICANCER AGENTS FROM TRADITIONAL CHINESE MEDICINE AND NATURAL PRODUCTS

Chemotherapy is still the effective strategy for treating cancer.It is important to explore anticancer agents from Traditional Chinese Medicine and Natural products.Different cancer cell lines were included in our research,such as HL60,K562,K562/ADR,KB,KBv200 cells.Cell growth inhibition assay,Annexin V-FITC/PI double-staining assay,measurement of reactive

UPLC-QTOF-MS FOR METABOLITES IDENTIFICATION IN CACO-2 CELLS OF BENZYLISOQUINOLINE ALKALOIDS IN NELUMBINIS PLUMULA

The aim of the study was to identify main metabolites of benzylisoquinoline alkaloids from Nelumbinis Plumula after biotransformation by Caco-2 cells.Caco-2 cells were seeded to a 6-well plate and cultured for a period of time until 80%of each well was filled with cells.Then,cell medium was replaced and the norcoclaurine,liensinine,isoliensinine and neferine were respectively added to