Objective To explore repair role of allogeneic bone marrow mesenchymal stem cells （BM-MSCs） transplantation on treating hepatic ischemia reperfusion injury （HIRI） in rats. Methods Ten rats were executed to get BM-MSCs， then BM-MSCs were cultured in vitro and dyed by 4，6-diamidino-2-phenylindole （DAPI）. Models of 70% hepatic ischemia reperfusion injury were eatablished. Thirty two rats were randomly divided into sham operation group （Sham group）， ischemia reperfusion group （I/R group）， Vitamin C group （VC group）， and BM-MSCs group. Serum samples were analyzed for ALT and AST， and hepatic tissue were for superoxide dismutase （SOD） and malondialdehyde （MDA）. Liver sections were stain with hematoxylin and eosin （HE） for histological analysis， TUNEL staining was applied to detect hepatic apoptosis. Serum and tissues were both collected at 24 h after reperfusion. Results The isolated BM-MSCs maintained vigorous growth in vitro. Specific markers for MSCs antigens CD29 and CD44 were detected by flow cytometry， but antigens CD34 and CD45 were not be detected. Models of HIRI were stable， and BM-MSCs were detected around the periportal area by DAPI staining. Compared with I/R group， levels of ALT， AST， MDA， and AI in the VC group and BM-MSCs group decreased at 24 h after reperfusion （P＜0.05）， meanwhile SOD level increased （P＜0.05）. Compared with VC group， levels of ALT， AST， MDA， and AI in the BM-MSC group decreased at 24 h after reperfusion （P＜0.05）， meanwhile SOD level increased （P＜0.05）. Conclusion BM-MSCs could protect HIRI by alleviating oxidative stress and inhibiting cellular apoptosis.
The aim of this study is to assess ischemia/reperfusion injury in carbon tetrachloride induced cirrhotic liver as compared to normal liver in the rats. Results showed that in cirrhotic liver, instead of diminishing the hepatic vein nitric oxide level increased significantly after ischemia from 8.04 μmol/L to 11.52 μmol/L and remained high till 5 hrs after reperfusion. The hepatic adenosine triphosphate (ATP) contents decreased as that seen in normal rat but did not restore to normal till the end of 5 hrs after reperfusion. Based on these findings, it is postulated that in cirrhotic liver, ischemia/reperfusion injury is aggrvated as evidenced by of nitric oxide, and extended diminishing in ATP.
目的 探讨磷丙泊酚钠后处理对大鼠肝脏缺血再灌注损伤的影响及是否呈剂量相关性。 方法 40只SD大鼠随机分为5组（每组n=8），即：假手术组（SP组）、生理盐水后处理组（NS组）、丙泊酚后处理组（PRO组）、低剂量磷丙泊酚钠[6 mg/（kg·h）]后处理组（LFOS组）、高剂量磷丙泊酚钠[12 mg/（kg·h）]后处理组（HFOS组）。除SP组外，其余4组在肝脏缺血60 min后给予药物后处理直至手术结束。在缺血60 min、再灌注60 min和120 min时采集血样，测定血清中丙氨酸氨基转移酶（ALT）、天门冬氨酸氨基转移酶（AST）、乳酸脱氢酶（ LDH）含量；在灌注120 min时取大鼠肝左外叶，用于HE染色，观察肝脏的形态学改变。 结果 与NS组相比，SP组、PRO组、LFOS组和HFOS组血清中的ALT、AST、LDH值明显降低（P＜0.05）；与SP组比较，PRO组、LFOS组、HFOS组和NS组的ALT、AST、LDH值升高（P＜0.05）；与PRO组比较，LFOS组的ALT、AST和LDH值差异无统计学意义（P＞0.05），HFOS组的ALT、AST和LDH值降低（P＜0.05）；LFOS组与HFOS组比较，HFOS组的ALT、AST和LDH值降低更为明显（P＜0.05）。 结论 磷丙泊酚钠后处理对大鼠肝脏缺血再灌注损伤具有保护作用，且高剂量磷丙泊酚钠[12 mg/（kg·h）]的保护作用更为明显，保护作用存在剂量依赖性。
ObjectiveTo investigate relationship between liver non-parenchymal cells and hepatic ischemia-reperfusion injury (HIRI).MethodThe relevant literatures on researches of the relationship between HIRI and liver non-parenchymal cells were analyzed and reviewed.ResultsDuring HIRI, hepatocytes could be severely damaged by aseptic inflammatory reaction and apoptosis. The liver non-parenchymal cells included Kupffer cells, sinusoidal endothelial cells, hepatic stellate cells, and dendritic cells, which could release a variety of cytokines and inflammatory mediators to promote the damage, and some liver non-parenchymal cells also had effect on reducing HIRI, for example: Kupffer cells could express heme oxygenase-1 to reduce HIRI, and hepatic stellate cells may participate in the repair process after HIRI. The role of liver non-parenchymal cells in HIRI was complex, but it also had potential therapeutic value.ConclusionLiver non-parenchymal cells can affect HIRI through a variety of mechanisms, which provide new goals and strategies for clinical reduction of HIRI.
ObjectiveTo summarize the research advances of pyroptosis in hepatic ischamia-reperfusion injury (IRI).MethodThe literatures about the studies of mechanism of pyroptosis in hepatic IRI were retrieved and analyzed.ResultsPyroptosis, also known as inflammatory necrocytosis, was proven to play an important role in the hepatic IRI. When hepatic ischemia-reperfusion occurred, the classical pathway of pyroptosis dependenting on caspase-1 and the non-classical pathway of pyroptosis dependenting on caspase-11 were initiated by specific stimulants, and leaded to the activation of gasdermin D, releases of proinflammatory factors such as interleukin-1β, interleukin-18, etc., and the recruitment and activation of neutrophils. Consequently, pyroptosis caused more severe hepatic inflammation and aggravated existing cell injury and dysfunction of liver during hepatic IRI.ConclusionsPyroptosis plays an important role in liver IRI. Further researches about mechanism of pyroptosis will be beneficial to the prevention and treatment of the pyroptosis of related diseases.