CAJ | 학술논문

背景:三氯化钆能抑制枯否细胞的活化,降低其吞噬活性,并减少枯否细胞激活后的肿瘤坏死因子α及白细胞介素1释放,从而减轻肝脏缺血再灌注损伤.目的:观察三氯化钆对大鼠移植肝缺血再灌注损伤的影响并探讨其作用机制.方法:供、受体均采用雄性 SD 大鼠,将实验动物随机分为3组.采用改良连续缝合进行肝上下腔静脉重建的 Kamada’s“两袖套法”建立大鼠肝移植模型.①假手术组:不行肝移植,游离肝脏、结扎静脉后关腹,不处理及用药.②生理盐水组:热缺血时间0-5 min,供肝冷保存时间为2 h,移植前连续3 d 经尾静脉向受鼠注射生理盐水,移植后再经尾静脉注射生理盐水1次.③三氯化钆组:热缺血时间为0-5 min,冷保存时间为2 h,移植前连续3 d 经尾静脉向受鼠注射0.5%三氯化钆,移植后再经尾静脉注射0.5%三氯化钆1次.24 h 后处死大鼠进行相应指标检测.结果与结论:与假手术组比较,三氯化钆组、生理盐水组血清丙氨酸转氨酶、谷氨酸转氨酶、碱性磷酸酶、γ-谷氨酰转移酶水平明显升高(P <0.05);三氯化钆组各指标较生理盐水组有所减轻(P <0.05).病理组织学检查发现生理盐水组、三氯化钆组病变范围及缺血再灌注损伤程度均较假手术组明显增加.与生理盐水组比较,三氯化钆组血清白细胞介素1、肿瘤坏死因子α及凋亡指数明显降低(P <0.05),淤血、空泡变性及坏死Suzuki’s评分均较低(P <0.05).提示三氯化钆在一定程度上是通过封闭枯否细胞吞噬并抑制细胞因子的释放实现对移植肝缺血再灌注损伤的保护机制.
배경:삼록화구능억제고부세포적활화,강저기탄서활성,병감소고부세포격활후적종류배사인자α급백세포개소1석방,종이감경간장결혈재관주손상.목적:관찰삼록화구대대서이식간결혈재관주손상적영향병탐토기작용궤제.방법:공、수체균채용웅성 SD 대서,장실험동물수궤분위3조.채용개량련속봉합진행간상하강정맥중건적 Kamada’s“량수투법”건립대서간이식모형.①가수술조:불행간이식,유리간장、결찰정맥후관복,불처리급용약.②생리염수조:열결혈시간0-5 min,공간랭보존시간위2 h,이식전련속3 d 경미정맥향수서주사생리염수,이식후재경미정맥주사생리염수1차.③삼록화구조:열결혈시간위0-5 min,랭보존시간위2 h,이식전련속3 d 경미정맥향수서주사0.5%삼록화구,이식후재경미정맥주사0.5%삼록화구1차.24 h 후처사대서진행상응지표검측.결과여결론:여가수술조비교,삼록화구조、생리염수조혈청병안산전안매、곡안산전안매、감성린산매、γ-곡안선전이매수평명현승고(P <0.05);삼록화구조각지표교생리염수조유소감경(P <0.05).병리조직학검사발현생리염수조、삼록화구조병변범위급결혈재관주손상정도균교가수술조명현증가.여생리염수조비교,삼록화구조혈청백세포개소1、종류배사인자α급조망지수명현강저(P <0.05),어혈、공포변성급배사Suzuki’s평분균교저(P <0.05).제시삼록화구재일정정도상시통과봉폐고부세포탄서병억제세포인자적석방실현대이식간결혈재관주손상적보호궤제.
BACKGROUND: Gadolinium chloride can inhibit the Kupffer cel activation, reduce their phagocytic activity, and reduce tumor necrosis factor alpha and interleukin 1 release after Kupffer cel activation, thereby al eviate the ischemia-reperfusion injury of liver. OBJECTIVE: To study the effect of gdolinium chloride on ischemia-reperfusion injury of rat receptor’s liver and to explore the mechanism. METHODS: Donors and receptors were al male Sprague Dawley rats which were randomly divided into three groups. The modified Kamada’s two-cuff technique was used to build rat liver transplantation model through liver superior and inferior vena cava reconstruction by modified continuous suture. In the sham-operation group, the rats were treated without liver transplantation, the liver was freed and the abdomen was closed after vein ligation without treatment and received drug administration. In the saline group, the warm ischemia time was 0-5 minutes and cold preservation time of the donor liver was 2 hours, the saline was injected into the rats via the tail vein for 3 days before implantation, and after implantation, the saline was injected into the rats once more. In the gadolinium chloride group, the warm ischemia time was 0-5 minutes and cold preservation time of the donor liver was 2 hours, 0.5% gadolinium chloride was injected into the rats via the tail vein for 3 days before implantation, and after implantation, the injection was performed once more. The rats were sacrificed after 24 hours for the corresponding index detection. RESULTS AND CONCLUSION: Compared with sham-operation group, the serum alanine aminotransferase, alanine aminotransferase, alkaline phosphatase and γ-gamma-glutamyl transferase levels were increased significantly in gadolinium chloride and saline groups (P < 0.05); al the indexes in gadolinium chloride group were decreased compared with saline group (P < 0.05). In pathologic histology tests, the lesion range and the extent of ischemia-reperfusion injury were al significantly increased in saline group and gadolinium chloride group. Compared with the saline group, the concentrations of interleukin-1, tumor necrosis factor-α and the apoptosis index were decreased significantly in gadolinium chloride group (P < 0.05), as wel as the congestion, vacuolar degeneration and Suzuki’s score (P < 0.05). The protective effect of gdolinium chloride on ischemia-reperfusion injury of receptor’s liver might result from closing the Kupffer cel s and reducing cytokine release.