本文選題：硫化氫 + 巨噬細(xì)胞　； 參考：《青海大學(xué)》2017年碩士論文

【摘要】：目的探討硫化氫對燒傷大鼠創(chuàng)面皮膚巨噬細(xì)胞體外培養(yǎng)分泌炎癥介質(zhì)TNF-α和IL-1β的影響方法探究對象選取經(jīng)過燒傷處理的大鼠背部創(chuàng)面皮膚巨噬細(xì)胞。取健康SD大鼠30只(雌雄不限),其中5只正常喂養(yǎng),余下25只實驗大鼠行燒傷造模后喂養(yǎng)。隨機選擇正常喂養(yǎng)大鼠中的1只設(shè)為正常對照組,燒傷造模處理大鼠中的12只設(shè)為燒傷實驗組。燒傷實驗組再隨機分成4組、每組3只,即燒傷對照組,Na HS(外源性H2S供體)組1h、6h、12h,格列本脲組(KATP通道阻滯劑)1h、6h、12h,Na HS+格列本脲組1h、6h、12h。燒傷實驗大鼠于背部全部制作成深I(lǐng)I°5%TBSA燒傷損傷(創(chuàng)面病理切片證實)的模型組,正常對照組大鼠不予任何處理,分離正常對照組大鼠背部皮膚及燒傷大鼠創(chuàng)面處皮膚基底巨噬細(xì)胞進行體外培養(yǎng)。在培養(yǎng)過程中,正常對照組與燒傷對照組巨噬細(xì)胞加入PBS液,Na HS組中加入濃度為200μmol/L的Na HS,格列本脲(Gli)組中加入濃度為200μmol/L的Gli,Na HS+Gli組中加入濃度為200μmol/L的Na HS和濃度為200μmol/L的Gli,于加入試劑之后的1h、6h、12h共3個時間點采取ELISA法檢測巨噬細(xì)胞體外培養(yǎng)上清液中TNF-α與IL-1β的含量。結(jié)果于各個相同時間點檢測,燒傷對照組巨噬細(xì)胞各時間點TNF-α與IL-1β的生成量均明顯高于正常對照組各對應(yīng)時間點生成量,差異明顯存在統(tǒng)計學(xué)意義(P0.05);Na HS組巨噬細(xì)胞各時間點TNF-α與IL-1β的生成量均低于燒傷對照組各對應(yīng)時間點生成量,差異明顯存在統(tǒng)計學(xué)意義(P0.05);格列本脲(Gli)組巨噬細(xì)胞各時間點TNF-α與IL-1β的生成量均高于燒傷對照組各對應(yīng)時間點生成量,差異明顯存在統(tǒng)計學(xué)意義(P0.05);Na HS組巨噬細(xì)胞各時間點TNF-α與IL-1β的生成量均低于Gli組各對應(yīng)時間點生成量,差異明顯存在統(tǒng)計學(xué)意義(P0.05);Na HS組巨噬細(xì)胞各時間點TNF-α與IL-1β的生成量均低于Na HS+Gli組各對應(yīng)時間點生成量,差異明顯存在統(tǒng)計學(xué)意義(P0.05)。Gli組巨噬細(xì)胞各時間點TNF-α與IL-1β的生成量均高于Na HS+Gli組各對應(yīng)時間點生成量,差異存在統(tǒng)計學(xué)意義(P0.05)。結(jié)論微量外源性H2S可減少燒傷創(chuàng)面巨噬細(xì)胞過量分泌炎癥介質(zhì)TNF-α和IL-1β,可降低燒傷后創(chuàng)面炎癥反應(yīng)程度。H2S憑借KATP通道途徑在巨噬細(xì)胞內(nèi)發(fā)揮其生理調(diào)節(jié)功能,格列本脲可憑借抑制KATP通道阻礙H2S產(chǎn)生生物學(xué)效應(yīng)。
[Abstract]:Objective to investigate the effects of hydrogen sulfide on the secretion of inflammatory mediators TNF- 偽 and IL-1 尾 by skin macrophages of burn rats in vitro. Thirty healthy SD rats (male and female) were selected. 5 of them were fed normally. The remaining 25 rats were fed with burn model. One of the normal feeding rats was randomly selected as the normal control group, and 12 of the burn model rats were set up as the burn experimental group. Burn experimental group was divided into 4 groups at random, 3 rats in each group, namely burn control group (external H 2S donor) group (1 h, 6 h, 12 h), glibenclamide group (1 h, 6 h, 12 h) and glibenclamide group (1 h, 6 h, 12 h). All the experimental rats were made into the model group of deep II 擄5%TBSA burn injury (confirmed by pathological section of the wound) in the back, while the normal control group did not receive any treatment. Basal macrophages were isolated from the dorsal skin of normal control rats and burn rats. In the process of cultivation, The macrophages of normal control group and burn control group were added to PBS solution NaHS group with 200 渭 mol/L NaHS, glibenclamide Glix group added 200 渭 mol/L Gligna Na HS Gli group and 200 渭 mol/L NaHS group and 200 渭 mol/L group respectively. The concentration of TNF- 偽 and IL-1 尾 in the supernatant of macrophages cultured in vitro was determined by ELISA method at 3 time points (1 h, 6 h and 12 h after reagents). Results the levels of TNF- 偽 and IL-1 尾 in macrophages in burn control group were significantly higher than those in normal control group at the same time points. There was significant difference in the amount of TNF- 偽 and IL-1 尾 in macrophages at different time points in P0.05An Na HS group, which was lower than that in burn control group at different time points. The difference was statistically significant (P 0.05), and the amount of TNF- 偽 and IL-1 尾 in the glibenclamide group was higher than that in the burn control group at each time point, and the content of TNF- 偽 and IL-1 尾 in the Glib group was higher than that in the burn control group at each time point. There was significant difference in the amount of TNF- 偽 and IL-1 尾 in macrophages at each time point in P0.05Na-Na HS group, which was lower than that in Gli group at different time points. There was significant difference in the amount of TNF- 偽 and IL-1 尾 in macrophages at each time point in P0.05Na-Na HS group, which was lower than that in Na HS Gli group at different time points. There was significant difference in the amount of TNF- 偽 and IL-1 尾 in macrophages at each time point in P0.05Gli group, which was significantly higher than that in Na HS Gli group at each time point. The difference was statistically significant (P 0.05). Conclusion Trace exogenous H2S can reduce the excessive secretion of inflammatory mediators TNF- 偽 and IL-1 尾 by burn wound macrophages, and reduce the degree of inflammatory response of burn wounds. H2S can play its physiological regulation function in macrophages by means of KATP channel pathway. Glibenclamide can inhibit the biological effect of H 2S by inhibiting KATP channel.
【學(xué)位授予單位】：青海大學(xué)
【學(xué)位級別】：碩士
【學(xué)位授予年份】：2017
【分類號】：R644

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