Majer-Piquet手术治疗声带癌的体会

Ｍａｊｅｒ－Ｐｉｑｕｅｔ手术是治疗Ｔ＿１、Ｔ＿２和个别Ｔ＿３声带癌有效的手术方法。手术切除肿瘤彻底、操作简便、同时能重建喉的发音装置。术后病人的呼吸、吞咽和发音功能恢复满意。本文介绍了手术方法，并就我科１８例手术病例的治疗效果和手术适应证作了讨论。     

肿瘤坏死因子相关诱导凋亡配体与放化疗联用对喉癌细胞的协同杀伤效应及机制

Objective To determine the sensitivity of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) induced apoptosis in Hep-2 cells by means of systematically evaluating the cytotoxicity of TRAIL alone and TRAIL in combination with chemotherapeutic agents (cisplatin, paclitaxel) or radiation in Hep-2 cells in vitro, and whether the synergistic killing effects correlated with the expression level of TRAIL receptors and the activity of caspnse-8 or caspase-9. Methods The cytotoxicities of TRAIL, cisplatin and paclitaxel were investigated by cell counting kit-8 (CCK-8) assay. The expression levels of four TRAIL receptors in Hep-2 cells after treated by TRAIL, chemotherapeutic agents or radiation alone and by combined treatments were measured by flow eytometry and Western blotting respectively. The growth inhibition effects of caspase-8 or caspase-9 inhibitor on Hep-2 cells were determined by CCK-8 assay, and the activities of caspase-8, caspase-9 and caspase-3 were measured by Western blotting. Results The half maximal inhibitory concentration(IC50) of TRAIL to Hep-2 ceils on 24 h was 596. 92 μg/L Cisplatin, paclitaxel and radiation had synergistic inhibitory effects with TRAIL on the growth of Hep-2 cell line. After the activity of caspase-9 was inhibited by Z-LETD-FMK, the inhibition effects of TRAIL, cisplatin and paclitaxel on Hep-2 cells decreased significantly (all P < 0. 05). The expressions of caspase-8, caspase-9 and the death receptors (DR4 and DR5) increased significantly (all P < 0. 05) after combined administration. Conclusions Hep-2 cells are resistant to the apoptosis induced by TRAIL and TRAIL can induce the apoptosis of Hep-2 cells through the endogenous apeptotic pathway. The increase of death receptors expression by chemotherapeutic agents or radiation could enhance the sensitivity of Hep-2 cells to TRAIL and the synergistic killing effects.     

肿瘤坏死因子相关诱导凋亡配体与放化疗联用对喉癌细胞的协同杀伤效应及机制

Objective To determine the sensitivity of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) induced apoptosis in Hep-2 cells by means of systematically evaluating the cytotoxicity of TRAIL alone and TRAIL in combination with chemotherapeutic agents (cisplatin, paclitaxel) or radiation in Hep-2 cells in vitro, and whether the synergistic killing effects correlated with the expression level of TRAIL receptors and the activity of caspnse-8 or caspase-9. Methods The cytotoxicities of TRAIL, cisplatin and paclitaxel were investigated by cell counting kit-8 (CCK-8) assay. The expression levels of four TRAIL receptors in Hep-2 cells after treated by TRAIL, chemotherapeutic agents or radiation alone and by combined treatments were measured by flow eytometry and Western blotting respectively. The growth inhibition effects of caspase-8 or caspase-9 inhibitor on Hep-2 cells were determined by CCK-8 assay, and the activities of caspase-8, caspase-9 and caspase-3 were measured by Western blotting. Results The half maximal inhibitory concentration(IC50) of TRAIL to Hep-2 ceils on 24 h was 596. 92 μg/L Cisplatin, paclitaxel and radiation had synergistic inhibitory effects with TRAIL on the growth of Hep-2 cell line. After the activity of caspase-9 was inhibited by Z-LETD-FMK, the inhibition effects of TRAIL, cisplatin and paclitaxel on Hep-2 cells decreased significantly (all P < 0. 05). The expressions of caspase-8, caspase-9 and the death receptors (DR4 and DR5) increased significantly (all P < 0. 05) after combined administration. Conclusions Hep-2 cells are resistant to the apoptosis induced by TRAIL and TRAIL can induce the apoptosis of Hep-2 cells through the endogenous apeptotic pathway. The increase of death receptors expression by chemotherapeutic agents or radiation could enhance the sensitivity of Hep-2 cells to TRAIL and the synergistic killing effects.     

肿瘤坏死因子相关诱导凋亡配体与放化疗联用对喉癌细胞的协同杀伤效应及机制

Objective To determine the sensitivity of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) induced apoptosis in Hep-2 cells by means of systematically evaluating the cytotoxicity of TRAIL alone and TRAIL in combination with chemotherapeutic agents (cisplatin, paclitaxel) or radiation in Hep-2 cells in vitro, and whether the synergistic killing effects correlated with the expression level of TRAIL receptors and the activity of caspnse-8 or caspase-9. Methods The cytotoxicities of TRAIL, cisplatin and paclitaxel were investigated by cell counting kit-8 (CCK-8) assay. The expression levels of four TRAIL receptors in Hep-2 cells after treated by TRAIL, chemotherapeutic agents or radiation alone and by combined treatments were measured by flow eytometry and Western blotting respectively. The growth inhibition effects of caspase-8 or caspase-9 inhibitor on Hep-2 cells were determined by CCK-8 assay, and the activities of caspase-8, caspase-9 and caspase-3 were measured by Western blotting. Results The half maximal inhibitory concentration(IC50) of TRAIL to Hep-2 ceils on 24 h was 596. 92 μg/L Cisplatin, paclitaxel and radiation had synergistic inhibitory effects with TRAIL on the growth of Hep-2 cell line. After the activity of caspase-9 was inhibited by Z-LETD-FMK, the inhibition effects of TRAIL, cisplatin and paclitaxel on Hep-2 cells decreased significantly (all P < 0. 05). The expressions of caspase-8, caspase-9 and the death receptors (DR4 and DR5) increased significantly (all P < 0. 05) after combined administration. Conclusions Hep-2 cells are resistant to the apoptosis induced by TRAIL and TRAIL can induce the apoptosis of Hep-2 cells through the endogenous apeptotic pathway. The increase of death receptors expression by chemotherapeutic agents or radiation could enhance the sensitivity of Hep-2 cells to TRAIL and the synergistic killing effects.     

肿瘤坏死因子相关诱导凋亡配体与放化疗联用对喉癌细胞的协同杀伤效应及机制

Objective To determine the sensitivity of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) induced apoptosis in Hep-2 cells by means of systematically evaluating the cytotoxicity of TRAIL alone and TRAIL in combination with chemotherapeutic agents (cisplatin, paclitaxel) or radiation in Hep-2 cells in vitro, and whether the synergistic killing effects correlated with the expression level of TRAIL receptors and the activity of caspnse-8 or caspase-9. Methods The cytotoxicities of TRAIL, cisplatin and paclitaxel were investigated by cell counting kit-8 (CCK-8) assay. The expression levels of four TRAIL receptors in Hep-2 cells after treated by TRAIL, chemotherapeutic agents or radiation alone and by combined treatments were measured by flow eytometry and Western blotting respectively. The growth inhibition effects of caspase-8 or caspase-9 inhibitor on Hep-2 cells were determined by CCK-8 assay, and the activities of caspase-8, caspase-9 and caspase-3 were measured by Western blotting. Results The half maximal inhibitory concentration(IC50) of TRAIL to Hep-2 ceils on 24 h was 596. 92 μg/L Cisplatin, paclitaxel and radiation had synergistic inhibitory effects with TRAIL on the growth of Hep-2 cell line. After the activity of caspase-9 was inhibited by Z-LETD-FMK, the inhibition effects of TRAIL, cisplatin and paclitaxel on Hep-2 cells decreased significantly (all P < 0. 05). The expressions of caspase-8, caspase-9 and the death receptors (DR4 and DR5) increased significantly (all P < 0. 05) after combined administration. Conclusions Hep-2 cells are resistant to the apoptosis induced by TRAIL and TRAIL can induce the apoptosis of Hep-2 cells through the endogenous apeptotic pathway. The increase of death receptors expression by chemotherapeutic agents or radiation could enhance the sensitivity of Hep-2 cells to TRAIL and the synergistic killing effects.     

肿瘤坏死因子相关诱导凋亡配体与放化疗联用对喉癌细胞的协同杀伤效应及机制

目的 探讨人喉癌Hep-2细胞对肿瘤坏死因子相关诱导凋亡配体(tumor necrosisfactor-related apoptosis-inducing ligand,TRAIL)诱导凋亡的敏感性,TRAIL与顺铂、紫杉醇、放射线联合应用对Hep-2细胞的杀伤效应及其调控机制.方法 采用活细胞计数试剂盒(cell counting kit-8,CCK-8)法检测TRAIL、顺铂、紫杉醇对Hep-2细胞的生长抑制率以及caspase-8、caspase-9抑制剂对其作用的影响;流式细胞仪检测Hep-2细胞凋亡率及TRAIL受体表达量;蛋白质印迹法检测联合用药后caspase-8、caspase-9、caspase-3及TRAIL受体表达变化.结果 TRAIL对Hep-2细胞的24 h半抑制浓度(half maximal inhibitory concentration,IC50)为596.92μg/L;顺铂、紫杉醇、放射线分别与TRAIL联合应用时Hep-2细胞凋亡率显著高于单药应用(P值均<0.05);caspase-9抑制剂Z-LETD-FMK使TRAIL、顺铂、紫杉醇对Hep-2细胞的生长抑制率显著下降(P值均<0.05);联合用药组caspase-8、caspase-9表达量显著升高,TRAIL死亡受体(DR4,DR5)表达量显著上调(P值均<0.05).结论人喉癌Hep-2细胞对TRAIL诱导的细胞凋亡不敏感,TRAIL通过内源性途径诱导Hep-2细胞凋亡;TRAIL死亡受体的表达上调可能增强了Hep-2细胞对TRAIL的敏感性,可能是联合用药对Hep-2细胞发挥协同效应的重要机制.喉肿瘤;癌,鳞状细胞;TNF相关凋亡诱导配体;细胞凋亡;药物协同作用;     

肿瘤坏死因子相关诱导凋亡配体与放化疗联用对喉癌细胞的协同杀伤效应及机制

Objective To determine the sensitivity of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) induced apoptosis in Hep-2 cells by means of systematically evaluating the cytotoxicity of TRAIL alone and TRAIL in combination with chemotherapeutic agents (cisplatin, paclitaxel) or radiation in Hep-2 cells in vitro, and whether the synergistic killing effects correlated with the expression level of TRAIL receptors and the activity of caspnse-8 or caspase-9. Methods The cytotoxicities of TRAIL, cisplatin and paclitaxel were investigated by cell counting kit-8 (CCK-8) assay. The expression levels of four TRAIL receptors in Hep-2 cells after treated by TRAIL, chemotherapeutic agents or radiation alone and by combined treatments were measured by flow eytometry and Western blotting respectively. The growth inhibition effects of caspase-8 or caspase-9 inhibitor on Hep-2 cells were determined by CCK-8 assay, and the activities of caspase-8, caspase-9 and caspase-3 were measured by Western blotting. Results The half maximal inhibitory concentration(IC50) of TRAIL to Hep-2 ceils on 24 h was 596. 92 μg/L Cisplatin, paclitaxel and radiation had synergistic inhibitory effects with TRAIL on the growth of Hep-2 cell line. After the activity of caspase-9 was inhibited by Z-LETD-FMK, the inhibition effects of TRAIL, cisplatin and paclitaxel on Hep-2 cells decreased significantly (all P < 0. 05). The expressions of caspase-8, caspase-9 and the death receptors (DR4 and DR5) increased significantly (all P < 0. 05) after combined administration. Conclusions Hep-2 cells are resistant to the apoptosis induced by TRAIL and TRAIL can induce the apoptosis of Hep-2 cells through the endogenous apeptotic pathway. The increase of death receptors expression by chemotherapeutic agents or radiation could enhance the sensitivity of Hep-2 cells to TRAIL and the synergistic killing effects.     

肿瘤坏死因子相关诱导凋亡配体与放化疗联用对喉癌细胞的协同杀伤效应及机制

Objective To determine the sensitivity of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) induced apoptosis in Hep-2 cells by means of systematically evaluating the cytotoxicity of TRAIL alone and TRAIL in combination with chemotherapeutic agents (cisplatin, paclitaxel) or radiation in Hep-2 cells in vitro, and whether the synergistic killing effects correlated with the expression level of TRAIL receptors and the activity of caspnse-8 or caspase-9. Methods The cytotoxicities of TRAIL, cisplatin and paclitaxel were investigated by cell counting kit-8 (CCK-8) assay. The expression levels of four TRAIL receptors in Hep-2 cells after treated by TRAIL, chemotherapeutic agents or radiation alone and by combined treatments were measured by flow eytometry and Western blotting respectively. The growth inhibition effects of caspase-8 or caspase-9 inhibitor on Hep-2 cells were determined by CCK-8 assay, and the activities of caspase-8, caspase-9 and caspase-3 were measured by Western blotting. Results The half maximal inhibitory concentration(IC50) of TRAIL to Hep-2 ceils on 24 h was 596. 92 μg/L Cisplatin, paclitaxel and radiation had synergistic inhibitory effects with TRAIL on the growth of Hep-2 cell line. After the activity of caspase-9 was inhibited by Z-LETD-FMK, the inhibition effects of TRAIL, cisplatin and paclitaxel on Hep-2 cells decreased significantly (all P < 0. 05). The expressions of caspase-8, caspase-9 and the death receptors (DR4 and DR5) increased significantly (all P < 0. 05) after combined administration. Conclusions Hep-2 cells are resistant to the apoptosis induced by TRAIL and TRAIL can induce the apoptosis of Hep-2 cells through the endogenous apeptotic pathway. The increase of death receptors expression by chemotherapeutic agents or radiation could enhance the sensitivity of Hep-2 cells to TRAIL and the synergistic killing effects.     

肿瘤坏死因子相关诱导凋亡配体与放化疗联用对喉癌细胞的协同杀伤效应及机制

Objective To determine the sensitivity of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) induced apoptosis in Hep-2 cells by means of systematically evaluating the cytotoxicity of TRAIL alone and TRAIL in combination with chemotherapeutic agents (cisplatin, paclitaxel) or radiation in Hep-2 cells in vitro, and whether the synergistic killing effects correlated with the expression level of TRAIL receptors and the activity of caspnse-8 or caspase-9. Methods The cytotoxicities of TRAIL, cisplatin and paclitaxel were investigated by cell counting kit-8 (CCK-8) assay. The expression levels of four TRAIL receptors in Hep-2 cells after treated by TRAIL, chemotherapeutic agents or radiation alone and by combined treatments were measured by flow eytometry and Western blotting respectively. The growth inhibition effects of caspase-8 or caspase-9 inhibitor on Hep-2 cells were determined by CCK-8 assay, and the activities of caspase-8, caspase-9 and caspase-3 were measured by Western blotting. Results The half maximal inhibitory concentration(IC50) of TRAIL to Hep-2 ceils on 24 h was 596. 92 μg/L Cisplatin, paclitaxel and radiation had synergistic inhibitory effects with TRAIL on the growth of Hep-2 cell line. After the activity of caspase-9 was inhibited by Z-LETD-FMK, the inhibition effects of TRAIL, cisplatin and paclitaxel on Hep-2 cells decreased significantly (all P < 0. 05). The expressions of caspase-8, caspase-9 and the death receptors (DR4 and DR5) increased significantly (all P < 0. 05) after combined administration. Conclusions Hep-2 cells are resistant to the apoptosis induced by TRAIL and TRAIL can induce the apoptosis of Hep-2 cells through the endogenous apeptotic pathway. The increase of death receptors expression by chemotherapeutic agents or radiation could enhance the sensitivity of Hep-2 cells to TRAIL and the synergistic killing effects.     

肿瘤坏死因子相关诱导凋亡配体与放化疗联用对喉癌细胞的协同杀伤效应及机制

Objective To determine the sensitivity of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) induced apoptosis in Hep-2 cells by means of systematically evaluating the cytotoxicity of TRAIL alone and TRAIL in combination with chemotherapeutic agents (cisplatin, paclitaxel) or radiation in Hep-2 cells in vitro, and whether the synergistic killing effects correlated with the expression level of TRAIL receptors and the activity of caspnse-8 or caspase-9. Methods The cytotoxicities of TRAIL, cisplatin and paclitaxel were investigated by cell counting kit-8 (CCK-8) assay. The expression levels of four TRAIL receptors in Hep-2 cells after treated by TRAIL, chemotherapeutic agents or radiation alone and by combined treatments were measured by flow eytometry and Western blotting respectively. The growth inhibition effects of caspase-8 or caspase-9 inhibitor on Hep-2 cells were determined by CCK-8 assay, and the activities of caspase-8, caspase-9 and caspase-3 were measured by Western blotting. Results The half maximal inhibitory concentration(IC50) of TRAIL to Hep-2 ceils on 24 h was 596. 92 μg/L Cisplatin, paclitaxel and radiation had synergistic inhibitory effects with TRAIL on the growth of Hep-2 cell line. After the activity of caspase-9 was inhibited by Z-LETD-FMK, the inhibition effects of TRAIL, cisplatin and paclitaxel on Hep-2 cells decreased significantly (all P < 0. 05). The expressions of caspase-8, caspase-9 and the death receptors (DR4 and DR5) increased significantly (all P < 0. 05) after combined administration. Conclusions Hep-2 cells are resistant to the apoptosis induced by TRAIL and TRAIL can induce the apoptosis of Hep-2 cells through the endogenous apeptotic pathway. The increase of death receptors expression by chemotherapeutic agents or radiation could enhance the sensitivity of Hep-2 cells to TRAIL and the synergistic killing effects.