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目的 研究盐酸右美托咪定(Dex)对脂多糖(LPS)诱导的库普弗细胞氧化应激和炎性反应的影响.方法 用雄性SD大鼠分离和培养肝库普弗细胞,将细胞随机分为6组:正常组、模型组、联合组、对照组和低、高2个剂量实验组.正常组常规培养,模型组细胞用1μg·m L-1LPS刺激3 h,低、高2个剂量实验组以模型细胞加0. 01,1μmol·L-1Dex培养24 h;联合组以模型细胞加1μmol·L-1Dex和100μmol·L-1育亨宾(α2肾上腺素能受体拮抗药)培养24 h;对照组以模型细胞加100μmol·L-1育亨宾培养24 h.用MTT法测定库普弗细胞存活率,用酶联免疫吸附法法测定库普弗细胞上清液中肿瘤坏死因子-α(TNF-α)、白细胞介素-6(IL-6)含量.结果 处置后,正常组、模型组、低与高2个剂量实验组、联合组和对照组的库普弗细胞存活率分别是(100. 00±0. 00)％,(56. 35±4. 21)％,(64. 78±4. 37)％,(83. 84±5. 16)％,(57. 03±4. 09)％和(54. 58±3. 95)％;这6组的TNF-α分别是(1. 19±0. 16),(57. 36±7. 23),(48. 27±5. 58),(7. 64±0. 92),(56. 98±7. 05)和(58. 03±7. 34)ng·m L-1;这6组的IL-6分别是(47. 38±6. 05),(289. 49±27. 83),(231. 17±22. 58),(85. 35±8. 23),(287. 96±26. 45)和(291. 43±28. 04)pg·m L-1.模型组正常组比较,上述指标差异均有统计学意义(均P <0. 05);低、高2个剂量实验组与模型组比较,上述指标差异均有统计学意义(均P <0. 05);联合组和对照组与低、高2个剂量实验组比较,上述指标差异均有统计学意义(均P <0. 05).结论 Dex能剂量依赖性地降低LPS诱导的库普弗细胞活性,抑制库普弗细胞引发的氧化应激损伤和炎性反应,其作用可能与激动α2肾上腺能受体有关,育亨宾对Dex疗效有拮抗作用.“,”Objective To study the effect of dexmedetomidine hydrochloride (Dex) on lipopolysaccharide (LPS) induced inflammatory response in Kupffer cells. Methods Healthy male SD rats were selected for isolation and culture of liver Kupffer cells. The cells were randomly divided into 6 groups: normal group, model group, experimental-L group, experimental-H group, combined group and control group. The normal group was cultured routinely, model group was cultured with 1μg·m L-1 LPS solution 3 h, experimental-L, experimental-H group were cultured respectively with 0. 01 μmol·L-1 or 1 μmol·L-1 Dex 24 h + 1 μg·m L-1 LPS solution 3 h, combined group was cultured with 1μmol·L-1 Dex + 100 μmol·L-1 yohimbine hydrochloride (α2 adrenergicreceptor antagonist) 24 h + 1 μg·m L-1 LPS 3 h, control group was cultured with 100 μmol·L-1 yohimbine hydrochloride 24 h. The survival rate of Kupffer cells was determined by MTT. The contents of tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) in the supernatant of Kupffer cells were determined by enzyme linked immunosorbent assay. Results After disposal, the survival rates of Kupffer cells in normal group, model group, experimental-L group, experimental-H group, combined group and control group were respectively (100. 00 ± 0. 00) ％, (56. 35 ± 4. 21) ％, (64. 78 ± 4. 37) ％, (83. 84 ± 5. 16) ％, (57. 03 ± 4. 09) ％ and (54. 58 ± 3. 95) ％. The TNF-αin the 6 groups were respectively (1. 19 ± 0. 16) , (57. 36 ± 7. 23) , (48. 27 ± 5. 58) , (7. 64 ± 0. 92) , (56. 98 ± 7. 05) and (58. 03 ± 7. 34) ng ·m L-1; the IL-6 in the 6 groups were respectively (47. 38 ± 6. 05) , (289. 49 ± 27. 83) , (231. 17 ± 22. 58) , (85. 35 ± 8. 23) , (287. 96 ± 26. 45) and (291. 43 ± 28. 04) pg·m L-1. Comparison between model group and normal group, the differences of the factors were significant (all P < 0. 05) ; comparison between two dose experimental groups and model group, the differences of the factors were significant (all P < 0. 05) ; comparison between combined group and control group with two dose experimental groups, the differences of the factors were significant (all P < 0. 05) . Conclusion Dex can reduce the activity of LPS induced Kupffer cells in a dose-dependent manner, inhibit oxidative stress injury and inflammatory response induced by Kupffer cells, which may be related to the agitation ofα2 adrenalic receptor. Yohimbine has antagonistic effect on its therapeutic effect.