Phytochemical profiling and anticancer potential of Cymbopogon citratus extract

Objective:To evaluate the anticancer potential of Cymbopogon citratus extract.Methods:GC-MS analysis was used to identify phytocomponents in the methanolic extract of Cymbopogon citratus.A fractionation method was employed to isolate and assess the bioactivity of different fractions and their cytotoxic activities against cancer cell lines HCT116,LoVo,Caco-2,and HT-29 were investigated.A dual staining method with acridine orange and ethidium bromide was used to assess the effect of the extract on cell apoptosis.Additionally,the expression levels of Bax and TP53 were quantified using real-time PCR in Caco-2 cells treated with the ethyl acetate fraction of Cymbopogon citratus extract.A protein array was employed to profile key pro-and anti-apoptotic proteins in Caco-2 cells.Moreover,molecular docking studies were conducted to investigate the interactions between key compounds of Cymbopogon citratus extract and specific apoptosis-related protein domains(PDB IDs:7wql and 4bkx).Results:A significant growth inhibition was observed in Caco-2 cells treated with Cymbopogon citratus extract.Among the seven fractions of the plant extract,the ethyl acetate fraction showed the highest cytotoxicity against Caco-2 cells with an IC50 value of(6.16±0.01)μg/mL.The immunofluorescence assay showed that the ethyl acetate fraction could induce apoptosis of Caco-2 cells.Moreover,the fraction upregulated the gene expressions of Bax and TP53 in a dose-dependent manner.The docking analysis demonstrated the interaction of five compounds isolated from the ethyl acetate fraction with key proteins in Caco-2 cells,indicating their anticancer properties.Conclusions:Cymbopogon citratus extract shows anticancer activity against Caco-2 cells by inducing apoptosis.It may be a promising candidate for the treatment of colon cancer,which needs further investigation.

由杂多钼酸盐前驱体制备的氧化钼催化剂催化CO_2存在下的异丁烷脱氢(英文)

Molybdenum based oxide catalysts Mo-H,Mo-Fe,Mo-Ce,and Mo-Sn were prepared by calcining H3PMo12O40,Fe1.5 PMo 12O40,Ce1.5PMo12O40,and Sn1.5 PMo12O40 heteropolyanion precursors at700℃,respectively.The prepared oxides have been characterized and tested for the dehydrogenation of isobutane(IB)to isobutene in the presence of CO2.The effects of temperature,time on stream,and CO2 /IB ratio were investigated.It was found that α-and-MoO3 phases were present in all catalysts.Catalytic tests showed that increasing the reaction temperature increased both the conversion and isobutene selectivity,whereas increasing the CO2 /IB molar ratio increased the conversion but decreased the selectivity for isobutene.Iron was found to be an effective additive element for the enhancement of catalytic activity compared with Ce and Sn.

Testosterone induced apoptosis in colon cancer cells is regulated by PI3K/Racl signaling

Recently, it has been reported that testosterone membrane signaling regulates actin reorganization and induces pro-apoptotic responses in colon tumor cells. In the present study the membrane androgen receptors （mARs）-induced activation of Rac I GTPase and the involvement of PI3K/Racl signaling in controlling the apoptotic responses in testosterone treated Caco2 colon cancer cells has been analyzed. In line with previous findings, activation of mAR by testosterone conjugates triggered early and transient actin reorganization as indicated by the significant decrease of the G/Total actin ratio after 15- and 30-min treatment of the cells. Interestingly, stimulation of mAR rapidly activated the Racl GTPase. This effect was evident after 15 min and persisted for at least 24 h. Testosterone induced Rac I activation was fully blocked in Caco2 cells pre-treated with the PI3K inhibitor wortmannin, indicating that Racl signaling is acting downstream of the PI3K pathway. Remarkably, when cells were pre-treated with wortmannin that blocks the PI3K/Racl signaling, apoptotic response was almost fully inhibited. These finding suggest that Racl activation, triggering actin redistribution, is involved in testosterone induced pro-apoptotic responses governed by mAR activation and emphasize the regulatory role of PI3K/Racl signaling in colon tumors.

Detection of oxidative stress and DNA damage in freshwater snail Lymnea leuteola exposed to profenofos

Extensive production and use of organophosphate pesticide in agriculture,has risen concerned about its ecotoxicity and risk assessment of insecticides,which are more important.Therefore,the present investigation was aimed to study the induction of oxidative stress and DNA damage by organophosphate insecticide profenofos(PFF)in freshwater snail Lymnea luteola(L.luteola).The median lethal value(96 h LC50)of PFF was estimated as 1.26 mg/L for L.luteola in a semi-static system and on the basis of LC50 value three concentrations viz.,0.126(1/10 of LC50,Sublethal I),0.63(1/2 of LC50,Sublethal II)and 0.84 mg/L(2/3 of LC50,Sublethal III)were determined.Snails were exposed to above-mentioned concentrations of PFF along with solvent control(acetone)and negative control for 96 h.The haemolymph was collected at 24 and 96 h of after treatment.In heamolymph of PFF exposed snail,lipid peroxide,glutathione reduced glutathione S transferase and superoxide dismutase activities at the tested concentrations significantly differ from those in the control.The genotoxicity induced in hemocytes of treated snails was measured by alkaline single cell gel electrophoresis assay.The data of this experiment demonstrated significantly enhancement of oxidative stress and DNA damage in the treated snails as compared to controls.Also,we observed statistically significant correlations of ROS with DNA damage(%tail DNA)(R^(2)=0.9708)for 24 h and DNA damage(R^(2)=0.9665)for 96 h.Results of the current experiment can be useful in risk evaluation of PFF among aquatic organisms.The study confirmed the use of comet assay for in vivo laboratory experiments using freshwater snail for selecting the toxic potential of industrial chemicals and environmental contaminants.