AIM: To explore the capability of a monoclonal antibody (mAb) against murine endoglin to inhibit tumor angiogenesis and suppression of hepatoma growth in murine models. METHODS: A monoclonal antibody against murine en...AIM: To explore the capability of a monoclonal antibody (mAb) against murine endoglin to inhibit tumor angiogenesis and suppression of hepatoma growth in murine models. METHODS: A monoclonal antibody against murine endoglin was purified by affinity chromatography and passively transfused through tail veins in two murine hepatoma models. Tumor volume and survival time were observed at three-day intervals for 48 d. Microvessels in tumor tissues were detected by immunohistochemistry against CD31, and angiogenesis in vivo was determined by alginate encapsulated assay. In addition, tumor cell apoptosis was detected by TUNEL assay. RESULTS: Passive immunotherapy with anti-endoglin mAb could effectively suppress tumor growth, and prolonged the survival time of hepatoma-bearing mice. Angiogenesis was apparently inhibited within the tumor tissues, and the vascularization of alginate beads was also reduced in the mice passively transfused with anti- endoglin mAb. In addition, increased apoptotic cells were observed within the tumor tissues from the mice passively transfused with anti-endoglin mAb. CONCLUSION: Passive immunotherapy with anti- endoglin mAb effectively inhibits tumor growth via inhibiting tumor angiogenesis and increasing tumor cell apoptosis, which may be highly correlated with the blockage of endoglin-related signal pathway induced bya nti-endoglin mAb.展开更多
Objective To investigate the main proteinases responsible for CD16b shedding under different stimulators. Methods HEK293 cell line stably expressing CD16b was constructed by lentivirus system. The cell line was then ...Objective To investigate the main proteinases responsible for CD16b shedding under different stimulators. Methods HEK293 cell line stably expressing CD16b was constructed by lentivirus system. The cell line was then overexpressed with a disintegrin and metalloproteinase 10 （ADAM10） or ADAM17, sup- pressed with short hairpin RNA of ADAM10 or ADAM I 7, and reconstituted with ADAM 10 or ADAM17, respectively. After each treatment, the cell line was stimulated with ionomycin or phorbol 12-myristate- 13-acetate （PMA） for 12 hours. The soluble CD 16b released from cell membrane was detected by immuno- precipition and immunoblot. Quantitation was then implemented to compare the amount of soluble CD 16b in cell supernatant after stimulation. Results HEK293 cell line stably expressing CD16b was successfully established. When CDI6b ex- pressing cell line was overexpressed with ADAM 10, shedding of CD 16b was increased after stimulation with ionomycin but not PMA; when the cell line overexpressed with ADAM I7, shedding of CDI6b was increased after stimulation with PMA but not ionomycin. Similarly, when ADAM10 was suppressed by short hairpin RNA, CD 16b shedding was decreased after stimulation with ionomycin; when ADAM 17 was suppressed by short hairpin RNA, CD16b shedding was decreased after stimulation with PMA. The shedding of CD16b was increased again when CD16b expressing cell line was reconstituted with ADAM10 and stimulated by ionomycin or reconstituted with ADAM 17 and stimulated by PMA. Conclusions Both ADAM10 and ADAM17 could shed CD16b, but they possess differed prefer- ences. ADAM10 is the main sheddase under stimulation of ionomycin, while ADAM17 is the main sheddase under stimulation of PMA.展开更多
Objective： To observe the effect of electroacupuncture （EA） gait function, and expression levels of serum immunoglobul intervertebral disc herniation （LIDH）. at Huantiao （GB 30） and Weizhong （BL 40） on thigme...Objective： To observe the effect of electroacupuncture （EA） gait function, and expression levels of serum immunoglobul intervertebral disc herniation （LIDH）. at Huantiao （GB 30） and Weizhong （BL 40） on thigmesthesia, n G （IgG） and immunoglobulin M （IgM） in rabbits with lumbar Methods： Forty healthy New Zealand rabbits were randomly divided into a blank control group, a model group, an EA at acupoint group and an EA at non-acupoint group, with 10 rabbits in each group. The LIDH pathological model of rabbit was established using the self-made LIDH model maker. The thigmesthesia and gait function of rabbits were recorded by Siegal method. The serum IgG and IgM expression levels were detected by enzyme-linked immunosorbent assay. Results： EA at Huantiao （GB 30） and Weizhong （BL 40） could improve the clinical symptoms of thigmesthesia and gait function, and inhibit the expressions of serum IgG and IgM in the LIDH rabbits, which were significantly different compared with those in the model group and EA at non-acupoint group. Conclusion： EA at Huantiao （GB 30） and Weizhong （BL 40） can improve the clinical symptoms of LIDH rabbits, which is associated with inhibition of the serum IgG and IgM expressions and reduction of the immunoinflammatory factor release. This may be one of the mechanisms of EA at Huantiao （GB 301 and Weizhong[BL 407 in the treatment of LIDH.展开更多
基金the National Natural Science Foundation of China, No. 30360115 and 30560048the Program for New Century Excellent Talents in University of China, No. NCET-05-0757the Foundation Project for Natural Science by the Education Department of Hainan Province of China, No. Hjkj200422
文摘AIM: To explore the capability of a monoclonal antibody (mAb) against murine endoglin to inhibit tumor angiogenesis and suppression of hepatoma growth in murine models. METHODS: A monoclonal antibody against murine endoglin was purified by affinity chromatography and passively transfused through tail veins in two murine hepatoma models. Tumor volume and survival time were observed at three-day intervals for 48 d. Microvessels in tumor tissues were detected by immunohistochemistry against CD31, and angiogenesis in vivo was determined by alginate encapsulated assay. In addition, tumor cell apoptosis was detected by TUNEL assay. RESULTS: Passive immunotherapy with anti-endoglin mAb could effectively suppress tumor growth, and prolonged the survival time of hepatoma-bearing mice. Angiogenesis was apparently inhibited within the tumor tissues, and the vascularization of alginate beads was also reduced in the mice passively transfused with anti- endoglin mAb. In addition, increased apoptotic cells were observed within the tumor tissues from the mice passively transfused with anti-endoglin mAb. CONCLUSION: Passive immunotherapy with anti- endoglin mAb effectively inhibits tumor growth via inhibiting tumor angiogenesis and increasing tumor cell apoptosis, which may be highly correlated with the blockage of endoglin-related signal pathway induced bya nti-endoglin mAb.
基金Supported by the National Natural Science Foundation of China (30872287)
文摘Objective To investigate the main proteinases responsible for CD16b shedding under different stimulators. Methods HEK293 cell line stably expressing CD16b was constructed by lentivirus system. The cell line was then overexpressed with a disintegrin and metalloproteinase 10 （ADAM10） or ADAM17, sup- pressed with short hairpin RNA of ADAM10 or ADAM I 7, and reconstituted with ADAM 10 or ADAM17, respectively. After each treatment, the cell line was stimulated with ionomycin or phorbol 12-myristate- 13-acetate （PMA） for 12 hours. The soluble CD 16b released from cell membrane was detected by immuno- precipition and immunoblot. Quantitation was then implemented to compare the amount of soluble CD 16b in cell supernatant after stimulation. Results HEK293 cell line stably expressing CD16b was successfully established. When CDI6b ex- pressing cell line was overexpressed with ADAM 10, shedding of CD 16b was increased after stimulation with ionomycin but not PMA; when the cell line overexpressed with ADAM I7, shedding of CDI6b was increased after stimulation with PMA but not ionomycin. Similarly, when ADAM10 was suppressed by short hairpin RNA, CD 16b shedding was decreased after stimulation with ionomycin; when ADAM 17 was suppressed by short hairpin RNA, CD16b shedding was decreased after stimulation with PMA. The shedding of CD16b was increased again when CD16b expressing cell line was reconstituted with ADAM10 and stimulated by ionomycin or reconstituted with ADAM 17 and stimulated by PMA. Conclusions Both ADAM10 and ADAM17 could shed CD16b, but they possess differed prefer- ences. ADAM10 is the main sheddase under stimulation of ionomycin, while ADAM17 is the main sheddase under stimulation of PMA.
基金supported by Scientific Research Project of Hunan Provincial Administration of Traditional Chinese Medicine,No.201378~~
文摘Objective： To observe the effect of electroacupuncture （EA） gait function, and expression levels of serum immunoglobul intervertebral disc herniation （LIDH）. at Huantiao （GB 30） and Weizhong （BL 40） on thigmesthesia, n G （IgG） and immunoglobulin M （IgM） in rabbits with lumbar Methods： Forty healthy New Zealand rabbits were randomly divided into a blank control group, a model group, an EA at acupoint group and an EA at non-acupoint group, with 10 rabbits in each group. The LIDH pathological model of rabbit was established using the self-made LIDH model maker. The thigmesthesia and gait function of rabbits were recorded by Siegal method. The serum IgG and IgM expression levels were detected by enzyme-linked immunosorbent assay. Results： EA at Huantiao （GB 30） and Weizhong （BL 40） could improve the clinical symptoms of thigmesthesia and gait function, and inhibit the expressions of serum IgG and IgM in the LIDH rabbits, which were significantly different compared with those in the model group and EA at non-acupoint group. Conclusion： EA at Huantiao （GB 30） and Weizhong （BL 40） can improve the clinical symptoms of LIDH rabbits, which is associated with inhibition of the serum IgG and IgM expressions and reduction of the immunoinflammatory factor release. This may be one of the mechanisms of EA at Huantiao （GB 301 and Weizhong[BL 407 in the treatment of LIDH.
