Cell death has been extensively evaluated for decades and it is well recognized that pharmacological interventions directed to inhibit cell death can prevent significant cell loss and can thus improve an organ�...Cell death has been extensively evaluated for decades and it is well recognized that pharmacological interventions directed to inhibit cell death can prevent significant cell loss and can thus improve an organ’s physiological function. For long, only apoptosis was considered as a sole form of programmed cell death. Recently necroptosis, a RIP1/RIP3-dependent programmed cell death, has been identified as an apoptotic backup cell death mechanism with necrotic morphology. The evidences of necroptosis and protective effects achieved by blocking necroptosis have been extensively reported in recent past. However, only a few studies reported the evidence of necroptosis and protective effects achieved by inhibiting necroptosis in liver related disease conditions. Although the number of necroptosis initiators is increasing; however, interestingly, it is still unclear that what actually triggers necroptosis in different liver diseases or if there is always a different necroptosis initiator in each specific disease condition followed by specific downstream signaling molecules. Understanding the precise mechanism of necroptosis as well as counteracting other cell death pathways in liver diseases could provide a useful insight towards achieving extensive therapeutic significance. By targeting necroptosis and/or other parallel death pathways, a significant cell loss and thus a decrement in an organ’s physiological function can be prevented.展开更多
OBJECTIVE： To investigate the anti-breast cancer （BC） effects and mechanisms of action of Xihuang pill （XHP） by conducting in vitro experiments on hu- man BC cell lines. METHODS： Two human BC cell lines （MCF-7 ...OBJECTIVE： To investigate the anti-breast cancer （BC） effects and mechanisms of action of Xihuang pill （XHP） by conducting in vitro experiments on hu- man BC cell lines. METHODS： Two human BC cell lines （MCF-7 and MDA- MB231） were cultured and treated with XHP. Cell viability was detected using the 3-（4, 5-Dimeth- ylthiazol-2-yl）-2, 5-diphenyltetrazolium bromide （MTT） assay. Flow cytometry was used to measure the cell cycle and apoptosis. The cell cycle was ana- lyzed with propidium iodide staining. Apoptosis was evaluated using the Annexin V-fluorescein iso- thiocyanate/propidium iodide method. Western blotting was used to analyze the expression of es- trogen receptor （ER）-α and ER-13.RESULTS： XHP had growth-inhibitory effects on MCF-7 and MDA-MB231 cells with a half-maximal inhibitory concentration （IC50） of 10.14 mg/mL （MCF-7） and 8.98 mg/mL （MDA-MB231）. Apoptosis was induced to some extent. Certain changes in the ER were caused. Upregulation of ER-a protein was found in MCF-7 cells. ER-β expression in MDA-MB231 cells was increased. Cell-cycle arrest was not observed in the two BC cell lines. ER-β ex- pression in MCF-7 cells was unchanged. No ER-a ex- pression was shown in MDA-MB231 cells. CONCLUSION： These data suggest that XHP can af- fect cell viability and cause apoptosis, but that the cell cycle is not blocked. XHP has a certain impact on ER expression, but its mechanisms of action of anti-13C effects may not be due to regulation of ER expression.展开更多
基金Supported by A grant of the Korea Healthcare technology R and D Project,Ministry of Health and Welfare,South Korea,NO.A121185
文摘Cell death has been extensively evaluated for decades and it is well recognized that pharmacological interventions directed to inhibit cell death can prevent significant cell loss and can thus improve an organ’s physiological function. For long, only apoptosis was considered as a sole form of programmed cell death. Recently necroptosis, a RIP1/RIP3-dependent programmed cell death, has been identified as an apoptotic backup cell death mechanism with necrotic morphology. The evidences of necroptosis and protective effects achieved by blocking necroptosis have been extensively reported in recent past. However, only a few studies reported the evidence of necroptosis and protective effects achieved by inhibiting necroptosis in liver related disease conditions. Although the number of necroptosis initiators is increasing; however, interestingly, it is still unclear that what actually triggers necroptosis in different liver diseases or if there is always a different necroptosis initiator in each specific disease condition followed by specific downstream signaling molecules. Understanding the precise mechanism of necroptosis as well as counteracting other cell death pathways in liver diseases could provide a useful insight towards achieving extensive therapeutic significance. By targeting necroptosis and/or other parallel death pathways, a significant cell loss and thus a decrement in an organ’s physiological function can be prevented.
基金Supported by the Beijing Traditional Chinese Medicine Science and Technology Project(QN2010-3)National Natural Science Foundation of China(No.81001564)
文摘OBJECTIVE： To investigate the anti-breast cancer （BC） effects and mechanisms of action of Xihuang pill （XHP） by conducting in vitro experiments on hu- man BC cell lines. METHODS： Two human BC cell lines （MCF-7 and MDA- MB231） were cultured and treated with XHP. Cell viability was detected using the 3-（4, 5-Dimeth- ylthiazol-2-yl）-2, 5-diphenyltetrazolium bromide （MTT） assay. Flow cytometry was used to measure the cell cycle and apoptosis. The cell cycle was ana- lyzed with propidium iodide staining. Apoptosis was evaluated using the Annexin V-fluorescein iso- thiocyanate/propidium iodide method. Western blotting was used to analyze the expression of es- trogen receptor （ER）-α and ER-13.RESULTS： XHP had growth-inhibitory effects on MCF-7 and MDA-MB231 cells with a half-maximal inhibitory concentration （IC50） of 10.14 mg/mL （MCF-7） and 8.98 mg/mL （MDA-MB231）. Apoptosis was induced to some extent. Certain changes in the ER were caused. Upregulation of ER-a protein was found in MCF-7 cells. ER-β expression in MDA-MB231 cells was increased. Cell-cycle arrest was not observed in the two BC cell lines. ER-β ex- pression in MCF-7 cells was unchanged. No ER-a ex- pression was shown in MDA-MB231 cells. CONCLUSION： These data suggest that XHP can af- fect cell viability and cause apoptosis, but that the cell cycle is not blocked. XHP has a certain impact on ER expression, but its mechanisms of action of anti-13C effects may not be due to regulation of ER expression.
