为了拓展藤黄在中医临床的应用,研究其内服的毒性及炮制减毒的机制是必要的。通过巨噬细胞RAW264.7释放炎症介质(一氧化氮NO、肿瘤坏死因子TNF-α和白细胞介素IL-6)和灌胃给予藤黄生品和炮制品后大鼠胃和十二指肠组织的病理表现,判断其...为了拓展藤黄在中医临床的应用,研究其内服的毒性及炮制减毒的机制是必要的。通过巨噬细胞RAW264.7释放炎症介质(一氧化氮NO、肿瘤坏死因子TNF-α和白细胞介素IL-6)和灌胃给予藤黄生品和炮制品后大鼠胃和十二指肠组织的病理表现,判断其毒性作用;采用免疫组化和实时荧光定量PCR技术检测灌胃给药后,大鼠胃和十二指肠组织AQP3,AQP4蛋白和m RNA的表达,研究藤黄炮制减毒的机制。结果表明,藤黄生品可促进炎症介质NO,TNF-α和IL-6的释放,且与剂量呈相关性;藤黄制品组与生品组比较,NO和IL-6的释放量降低,TNF-α的释放量增加;藤黄生品可引起大鼠腹泻、白细胞升高、淋巴细胞降低,使胃黏膜充血水肿,肠黏膜坏死和炎细胞浸润,从多个角度证明内服生藤黄对胃和十二指肠组织的毒性为致炎毒性,致炎毒性与给药剂量呈相关性,炮制后藤黄的致炎毒性降低。在藤黄对胃和十二指肠组织致炎的同时,藤黄生品高剂量组大鼠胃和十二指肠组织水通道蛋白AQP3,AQP4 m RNA和蛋白表达量显著增加(P<0.05),相应剂量藤黄制品组大鼠AQP3,AQP4表达量较生藤黄组低,说明AQP3,AQP4蛋白和m RNA表达量的高低与藤黄的致炎作用强弱有一致性。通过降低AQP3,AQP4的表达水平可能是藤黄炮制减毒的作用机制之一。展开更多
目的:探讨止痛润肠浓煎饮防治混合痔术后便秘的机制。方法:将48只SD大鼠随机分为:A组(正常组)、B组(模型组)、C组(麻仁软胶囊组)和D、E、F组(止痛润肠浓煎饮低、中、高剂量组)。治疗后测算小肠活性炭凝胶推进长度和推进率;检测血清前列...目的:探讨止痛润肠浓煎饮防治混合痔术后便秘的机制。方法:将48只SD大鼠随机分为:A组(正常组)、B组(模型组)、C组(麻仁软胶囊组)和D、E、F组(止痛润肠浓煎饮低、中、高剂量组)。治疗后测算小肠活性炭凝胶推进长度和推进率;检测血清前列腺素E2(PGE2)水平;RT-PCR检测结肠水通道蛋白3(AQP3)m RNA表达水平;免疫组化检测结肠黏膜AQP3蛋白表达情况。结果:与B组比较,各治疗组小肠活性炭凝胶推进长度和推进率均提高(P<0.01);E、F组PGE2水平下降(P<0.01);C、D、E、F组AQP3 m RNA表达水平均上调(P<0.01);E、F组AQP3蛋白表达上调(P<0.01)。结论:止痛润肠浓煎饮可能通过促进肠蠕动、减轻肛门疼痛、调节AQP3表达等防治混合痔术后便秘。展开更多
Violence against the neck can result in a range of macromorphological and micromorphological findings.However,the forensic relevance of the carotid sinus in cases of violence against the neck remains controversial.In ...Violence against the neck can result in a range of macromorphological and micromorphological findings.However,the forensic relevance of the carotid sinus in cases of violence against the neck remains controversial.In this follow-up study of 22 cases of suicidal and accidental strangulations,carotid bifurcations were examined histologically for morphological changes implying direct trauma,including haemorrhage and immunohistochemical expression of heat-shock proteins 27,60,and 70 and aquaporin-3.These cases were compared with a control group(82 cases)without neck compression or head trauma and with variable causes of death.No relevant histopathological findings implying direct trauma of the carotid bifurcation were found.No cases showed positive aquaporin-3 staining and only five cases showed positive heat-shock protein-27 staining,all of which were hangings.Without massive trauma of the carotid bifurcation,histological alterations cannot be expected.Without signs of rapid death,findings of acute circulatory failure,macromorphological and micromorphological findings of neck compression,and reliable markers indicating relevant impact on the carotid bifurcation the diagnosis of a lethal reflex cannot be verified.展开更多
文摘为了拓展藤黄在中医临床的应用,研究其内服的毒性及炮制减毒的机制是必要的。通过巨噬细胞RAW264.7释放炎症介质(一氧化氮NO、肿瘤坏死因子TNF-α和白细胞介素IL-6)和灌胃给予藤黄生品和炮制品后大鼠胃和十二指肠组织的病理表现,判断其毒性作用;采用免疫组化和实时荧光定量PCR技术检测灌胃给药后,大鼠胃和十二指肠组织AQP3,AQP4蛋白和m RNA的表达,研究藤黄炮制减毒的机制。结果表明,藤黄生品可促进炎症介质NO,TNF-α和IL-6的释放,且与剂量呈相关性;藤黄制品组与生品组比较,NO和IL-6的释放量降低,TNF-α的释放量增加;藤黄生品可引起大鼠腹泻、白细胞升高、淋巴细胞降低,使胃黏膜充血水肿,肠黏膜坏死和炎细胞浸润,从多个角度证明内服生藤黄对胃和十二指肠组织的毒性为致炎毒性,致炎毒性与给药剂量呈相关性,炮制后藤黄的致炎毒性降低。在藤黄对胃和十二指肠组织致炎的同时,藤黄生品高剂量组大鼠胃和十二指肠组织水通道蛋白AQP3,AQP4 m RNA和蛋白表达量显著增加(P<0.05),相应剂量藤黄制品组大鼠AQP3,AQP4表达量较生藤黄组低,说明AQP3,AQP4蛋白和m RNA表达量的高低与藤黄的致炎作用强弱有一致性。通过降低AQP3,AQP4的表达水平可能是藤黄炮制减毒的作用机制之一。
文摘目的:探讨止痛润肠浓煎饮防治混合痔术后便秘的机制。方法:将48只SD大鼠随机分为:A组(正常组)、B组(模型组)、C组(麻仁软胶囊组)和D、E、F组(止痛润肠浓煎饮低、中、高剂量组)。治疗后测算小肠活性炭凝胶推进长度和推进率;检测血清前列腺素E2(PGE2)水平;RT-PCR检测结肠水通道蛋白3(AQP3)m RNA表达水平;免疫组化检测结肠黏膜AQP3蛋白表达情况。结果:与B组比较,各治疗组小肠活性炭凝胶推进长度和推进率均提高(P<0.01);E、F组PGE2水平下降(P<0.01);C、D、E、F组AQP3 m RNA表达水平均上调(P<0.01);E、F组AQP3蛋白表达上调(P<0.01)。结论:止痛润肠浓煎饮可能通过促进肠蠕动、减轻肛门疼痛、调节AQP3表达等防治混合痔术后便秘。
文摘Violence against the neck can result in a range of macromorphological and micromorphological findings.However,the forensic relevance of the carotid sinus in cases of violence against the neck remains controversial.In this follow-up study of 22 cases of suicidal and accidental strangulations,carotid bifurcations were examined histologically for morphological changes implying direct trauma,including haemorrhage and immunohistochemical expression of heat-shock proteins 27,60,and 70 and aquaporin-3.These cases were compared with a control group(82 cases)without neck compression or head trauma and with variable causes of death.No relevant histopathological findings implying direct trauma of the carotid bifurcation were found.No cases showed positive aquaporin-3 staining and only five cases showed positive heat-shock protein-27 staining,all of which were hangings.Without massive trauma of the carotid bifurcation,histological alterations cannot be expected.Without signs of rapid death,findings of acute circulatory failure,macromorphological and micromorphological findings of neck compression,and reliable markers indicating relevant impact on the carotid bifurcation the diagnosis of a lethal reflex cannot be verified.
