目的 :探讨肾康注射液对肾小管上皮细胞 L L C PK1 分泌 型胶原 (Co )的影响。方法 :用细胞酶联免疫吸附法 (EL ISA ) ,以单味大黄注射液为实验对照组 ,检测肾康注射液对肾小管上皮细胞 L L C PK1 分泌Co 含量的影响。结果 :肾康注射...目的 :探讨肾康注射液对肾小管上皮细胞 L L C PK1 分泌 型胶原 (Co )的影响。方法 :用细胞酶联免疫吸附法 (EL ISA ) ,以单味大黄注射液为实验对照组 ,检测肾康注射液对肾小管上皮细胞 L L C PK1 分泌Co 含量的影响。结果 :肾康注射液可以显著抑制肾小管上皮细胞 L L C PK1 分泌 Co 的含量 ,并呈剂量依赖关系 ;肾康注射液作用明显优于同等含量的单味大黄注射液。结论 :肾康注射液抑制肾小管上皮细胞 L L CPK1 分泌 Co 含量 ,是该中药复方延缓慢性肾功能衰竭进展的机制之一。展开更多
目的 :探讨细胞培养液中有、无小牛血清对镉诱导猪肾近曲小管上皮细胞 (L L C-PK1 )损伤的影响 ,为研究镉对 L L C- PK1 细胞毒性的方法提供依据。方法 :用四甲基偶氮唑盐(MTT)比色法比较有、无小牛血清细胞存活率 ,Im age- Pro Plus软...目的 :探讨细胞培养液中有、无小牛血清对镉诱导猪肾近曲小管上皮细胞 (L L C-PK1 )损伤的影响 ,为研究镉对 L L C- PK1 细胞毒性的方法提供依据。方法 :用四甲基偶氮唑盐(MTT)比色法比较有、无小牛血清细胞存活率 ,Im age- Pro Plus软件系统拍摄有、无血清细胞光学形态变化。结果 :相同浓度 Cd Cl2 作用 8h、12 h后 ,有血清条件下的细胞存活率高于无血清条件下的存活率。无血清条件下 ,4 0μmol/ L Cd Cl2 作用 L L C- PK1 细胞 12 h,视野下几乎全部为悬浮细胞 ;有血清的条件下 ,4 0μmol/ L Cd Cl2 作用下 12 h,部分细胞悬浮 ,大多为正常贴壁细胞。结论 :血清可明显抑制镉对 L L C- PK1 细胞毒性效应 ,在研究镉体外培养细胞毒性的实验中 ,采用无血清条件为宜。展开更多
Objective To explore the effect of chronic hypoxia on the proliferation and differentiation of LLCPK, cells. Methods: The cells were exposed either to hypoxia (3 % O2) or maintained in normoxia (18 % O2 )followed by t...Objective To explore the effect of chronic hypoxia on the proliferation and differentiation of LLCPK, cells. Methods: The cells were exposed either to hypoxia (3 % O2) or maintained in normoxia (18 % O2 )followed by the assessment of [3H]-thymidine incorporation and cell number as indices of cellular proliferation and sodium - dependent transport of glucose and aminoisobutyric acid (AIB) as indices of differentiation.Protein kinase C (PKC ) was determined with radionuclear technique. Results: Exposure of quiescent culturesto hypoxia for 16 h resulted in a significant increase in [3H]-thymldine followed by a significant increase incell number at 24 h in comparison with respective normoxic controls. Confluent cultures exposed to 72 h ofhypoxia exhibited significant inhibition of α--methyl glucose and AIB uptakes when compared with their respective norrnoxic counterparts. Hypoxia also activated PKC at 4 h followed by a subsequent return to baseline with reactivation at 24 h which remained sustained up to 72 h, suggesting a biphasic acute and sustainedactivation of PKC. Furthermore, the hypoxia--induced alterations in [H]-thymidine incorporation as well asα-methyl glucose and AId transport activities were mitigated by inhibitors of PKC. Conclusion: Chronic hypoxia induces both proliferation and dedifferentiation of LLC-PK, cells mediated, in part, by the sustained activation of PKC.展开更多
文摘目的 :探讨肾康注射液对肾小管上皮细胞 L L C PK1 分泌 型胶原 (Co )的影响。方法 :用细胞酶联免疫吸附法 (EL ISA ) ,以单味大黄注射液为实验对照组 ,检测肾康注射液对肾小管上皮细胞 L L C PK1 分泌Co 含量的影响。结果 :肾康注射液可以显著抑制肾小管上皮细胞 L L C PK1 分泌 Co 的含量 ,并呈剂量依赖关系 ;肾康注射液作用明显优于同等含量的单味大黄注射液。结论 :肾康注射液抑制肾小管上皮细胞 L L CPK1 分泌 Co 含量 ,是该中药复方延缓慢性肾功能衰竭进展的机制之一。
文摘目的 :探讨细胞培养液中有、无小牛血清对镉诱导猪肾近曲小管上皮细胞 (L L C-PK1 )损伤的影响 ,为研究镉对 L L C- PK1 细胞毒性的方法提供依据。方法 :用四甲基偶氮唑盐(MTT)比色法比较有、无小牛血清细胞存活率 ,Im age- Pro Plus软件系统拍摄有、无血清细胞光学形态变化。结果 :相同浓度 Cd Cl2 作用 8h、12 h后 ,有血清条件下的细胞存活率高于无血清条件下的存活率。无血清条件下 ,4 0μmol/ L Cd Cl2 作用 L L C- PK1 细胞 12 h,视野下几乎全部为悬浮细胞 ;有血清的条件下 ,4 0μmol/ L Cd Cl2 作用下 12 h,部分细胞悬浮 ,大多为正常贴壁细胞。结论 :血清可明显抑制镉对 L L C- PK1 细胞毒性效应 ,在研究镉体外培养细胞毒性的实验中 ,采用无血清条件为宜。
文摘Objective To explore the effect of chronic hypoxia on the proliferation and differentiation of LLCPK, cells. Methods: The cells were exposed either to hypoxia (3 % O2) or maintained in normoxia (18 % O2 )followed by the assessment of [3H]-thymidine incorporation and cell number as indices of cellular proliferation and sodium - dependent transport of glucose and aminoisobutyric acid (AIB) as indices of differentiation.Protein kinase C (PKC ) was determined with radionuclear technique. Results: Exposure of quiescent culturesto hypoxia for 16 h resulted in a significant increase in [3H]-thymldine followed by a significant increase incell number at 24 h in comparison with respective normoxic controls. Confluent cultures exposed to 72 h ofhypoxia exhibited significant inhibition of α--methyl glucose and AIB uptakes when compared with their respective norrnoxic counterparts. Hypoxia also activated PKC at 4 h followed by a subsequent return to baseline with reactivation at 24 h which remained sustained up to 72 h, suggesting a biphasic acute and sustainedactivation of PKC. Furthermore, the hypoxia--induced alterations in [H]-thymidine incorporation as well asα-methyl glucose and AId transport activities were mitigated by inhibitors of PKC. Conclusion: Chronic hypoxia induces both proliferation and dedifferentiation of LLC-PK, cells mediated, in part, by the sustained activation of PKC.
