中南大学学报（医学版）
中南大學學報（醫學版）
중남대학학보（의학판）
JOURNAL OF CENTRAL SOUTH UNIVERSITY (MEDICAL SCIENCES)
2013年
10期
1014-1019
,共6页
蒋丽丽%齐择优%李李%沈金美
蔣麗麗%齊擇優%李李%瀋金美
장려려%제택우%리리%침금미
右美托咪定%氧化应激%肺泡巨噬细胞
右美託咪定%氧化應激%肺泡巨噬細胞
우미탁미정%양화응격%폐포거서세포
dexmedetomidine%oxidative stress%alveolar macrophages
目的：观察α2肾上腺素受体激动剂盐酸右美托咪定是否能够对抗过氧化氢(H2O2)诱导的肺泡巨噬细胞氧化损伤。方法：选择合适浓度H2O2和作用时间建立细胞氧化损伤模型，应用0.01，0.10，1.00μmol/L浓度盐酸右美托咪定分别处理24 h后，再应用MTT比色法检测H2O2诱导的损伤细胞的存活率；用相应试剂盒测定细胞乳酸脱氢酶(lactate dehydrogenase，LDH)和肿瘤坏死因子-α(TNF-α)释放量。结果：50~300μmol/L H2O2浓度依赖性地引起肺泡巨噬细胞氧化损伤，降低细胞存活率，增加LDH和TNF-α释放。0.01~1.00μmol/L盐酸右美托咪定可以浓度依赖性地对抗H2O2诱导的细胞氧化损伤，使细胞存活率明显增加，减少LDH和TNF-α释放，这种作用具有剂量依赖性。α2受体拮抗剂育亨宾能够完全拮抗盐酸右美托咪定的这种保护作用，并且育亨宾本身对细胞的氧化损伤没有影响。结论：盐酸右美托咪定能保护肺泡巨噬细胞对抗H2O2诱导的氧化应激损伤，此作用可能通过α2肾上腺素受体发挥作用。
目的：觀察α2腎上腺素受體激動劑鹽痠右美託咪定是否能夠對抗過氧化氫(H2O2)誘導的肺泡巨噬細胞氧化損傷。方法：選擇閤適濃度H2O2和作用時間建立細胞氧化損傷模型，應用0.01，0.10，1.00μmol/L濃度鹽痠右美託咪定分彆處理24 h後，再應用MTT比色法檢測H2O2誘導的損傷細胞的存活率；用相應試劑盒測定細胞乳痠脫氫酶(lactate dehydrogenase，LDH)和腫瘤壞死因子-α(TNF-α)釋放量。結果：50~300μmol/L H2O2濃度依賴性地引起肺泡巨噬細胞氧化損傷，降低細胞存活率，增加LDH和TNF-α釋放。0.01~1.00μmol/L鹽痠右美託咪定可以濃度依賴性地對抗H2O2誘導的細胞氧化損傷，使細胞存活率明顯增加，減少LDH和TNF-α釋放，這種作用具有劑量依賴性。α2受體拮抗劑育亨賓能夠完全拮抗鹽痠右美託咪定的這種保護作用，併且育亨賓本身對細胞的氧化損傷沒有影響。結論：鹽痠右美託咪定能保護肺泡巨噬細胞對抗H2O2誘導的氧化應激損傷，此作用可能通過α2腎上腺素受體髮揮作用。
목적：관찰α2신상선소수체격동제염산우미탁미정시부능구대항과양화경(H2O2)유도적폐포거서세포양화손상。방법：선택합괄농도H2O2화작용시간건립세포양화손상모형，응용0.01，0.10，1.00μmol/L농도염산우미탁미정분별처리24 h후，재응용MTT비색법검측H2O2유도적손상세포적존활솔；용상응시제합측정세포유산탈경매(lactate dehydrogenase，LDH)화종류배사인자-α(TNF-α)석방량。결과：50~300μmol/L H2O2농도의뢰성지인기폐포거서세포양화손상，강저세포존활솔，증가LDH화TNF-α석방。0.01~1.00μmol/L염산우미탁미정가이농도의뢰성지대항H2O2유도적세포양화손상，사세포존활솔명현증가，감소LDH화TNF-α석방，저충작용구유제량의뢰성。α2수체길항제육형빈능구완전길항염산우미탁미정적저충보호작용，병차육형빈본신대세포적양화손상몰유영향。결론：염산우미탁미정능보호폐포거서세포대항H2O2유도적양화응격손상，차작용가능통과α2신상선소수체발휘작용。
Objective: To evaluate whether dexmedetomidine hydrochloride, an α2-adrenergic receptor agonist, can prevent oxidative damage to alveolar macrophages induced by H2O2.
<br> Methods: We used methyl thiazolyl tetrazolium (MTT) colorimetry to test the effect of different concentrations and action time of H2O2 on the survival rate of alveolar macrophages, and then we chose the appropriate H2O2 concentration and action time to build NR8383 cell oxidative damage model. After pre-conditioning of 0.01, 0.10, and 1.00 μmol/L dexmedetomidine hydrochloride for 24 hours, MTT colorimetry was used to demonstrate the survival rate of NR8383 cells damaged by H2O2, and the release of lactate dehydrogenase (LDH) and TNF-α by H2O2-damaged NR8383 cells was detected by corresponding kit.
<br> Results: At 50-300 μmol/L, H2O2 caused concentration-dependent oxidative damage in the alveolar macrophages, decreased the cell survival rate, and increased LDH and TNF-α release. At 0.01-1.00 μmol/L dexmedetomidine hydrochloride concentration-dependently protected NR8383 cells from oxidative damage induced by H2O2, significantly increased the cell survival rate, decreased LDH and TNF-α release, and this effect of dexmedetomidine hydrochloride was dose-dependent. Yohimbine, an α2 - adrenergic receptor antagonist, completely neutralized the protective effect of dexmedetomidine hydrochloride on NR8383 cells without affecting the oxidative damage of NR8383 cells.
<br> Conclusion: Dexmedetomidine hydrochloride can prevent alveolar macrophages from oxidative damage induced by H2O2, which may play a protective role through α2 - adrenergic receptors.
