Effect of conditioned medium from adipose derived mesenchymal stem cells on endoplasmic reticulum stress and lipid metabolism after hepatic ischemia reperfusion injury and hepatectomy in swine

Life Sciences ◽  
2021 ◽  
pp. 120212
Author(s):  
Qianzhen Zhang ◽  
Xiaoning Liu ◽  
Chenxi Piao ◽  
Zhihui Jiao ◽  
Yajun Ma ◽  
...  
Keyword(s):  
Stem Cells ◽  
Endoplasmic Reticulum ◽  
Mesenchymal Stem Cells ◽  
Lipid Metabolism ◽  
Endoplasmic Reticulum Stress ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Hepatic Ischemia ◽  
Hepatic Ischemia Reperfusion

scholarly journals Fate and Effect of Intravenously Infused Mesenchymal Stem Cells in a Mouse Model of Hepatic Ischemia Reperfusion Injury and Resection

2016 ◽  
Vol 2016 ◽  
pp. 1-9 ◽  
Author(s):  
T. C. Saat ◽  
S. van den Engel ◽  
W. Bijman-Lachger ◽  
S. S. Korevaar ◽  
M. J. Hoogduijn ◽  
...  
Keyword(s):  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Weight Ratio ◽  
Hepatocellular Injury ◽  
Hepatic Ischemia ◽  
Beneficial Effects ◽  
Hepatic Ischemia Reperfusion

Liver ischemia reperfusion injury (IRI) is inevitable during transplantation and resection and is characterized by hepatocellular injury. Therapeutic strategies to reduce IRI and accelerate regeneration could offer major benefits. Mesenchymal stem cells (MSC) are reported to have anti-inflammatory and regeneration promoting properties. We investigated the effect of MSC in a model of combined IRI and partial resection in the mouse. Hepatic IRI was induced by occlusion of 70% of the blood flow during 60 minutes, followed by 30% hepatectomy. 2 × 105MSC or PBS were infused 2 hours before or 1 hour after IRI. Six, 48, and 120 hours postoperatively mice were sacrificed. Liver damage was evaluated by liver enzymes, histology, and inflammatory markers. Regeneration was determined by liver/body weight ratio, proliferating hepatocytes, and TGF-βlevels. Fate of MSC was visualized with 3D cryoimaging. Infusion of 2 × 105MSC 2 hours before or 1 hour after IRI and resection showed no beneficial effects. Tracking revealed that MSC were trapped in the lungs and did not migrate to the site of injury and many cells had already disappeared 2 hours after infusion. Based on these findings we conclude that intravenously infused MSC disappear rapidly and were unable to induce beneficial effects in a clinically relevant model of IRI and resection.

scholarly journals Dexmedetomidine Protects against Hepatic Ischemia-Reperfusion Injury by inhibiting Endoplasmic Reticulum Stress and Cell Apoptosis in Rats

2021 ◽  
Author(s):  
Hang Li ◽  
Jilang Tang ◽  
Weiqi Zhang ◽  
Liping Ai ◽  
Shixia Zhang
Keyword(s):  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress ◽  
Protective Effect ◽  
Reperfusion Injury ◽  
Cell Apoptosis ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Hepatic Ischemia ◽  
Significant Difference ◽  
Hepatic Ischemia Reperfusion

Abstract Background: Hepatic ischemia-reperfusion injury (IRI) remains a major complication of liver surgery, dexmedetomidine (DEX) has a certain protective effect on liver during ischemia-reperfusion, but the underlying mechanisms are not fully understood. This study explored the protective effects of DEX and investigated whether DEX protects against hepatic IRI by inhibiting endoplasmic reticulum stress (ERS) and its downstream apoptotic pathway in a rat model. Methods: Thirty-six male Sprague-Dawley (SD) rats were divided into six groups: S, IR, DL, DM1, DH and DM2 group. Group S was subjected to laparotomy, and exposure of the portal triad without occlusion. I-R injury model was induced by clamping the portal vessels supplying the middle and left hepatic lobes for 30 min in IR, DL, DM1, DH and DM2 group. Then DL, DM1, DH group received DEX of 25 μg/kg, 50 μg/kg and 100 μg/kg intraperitoneally at 30 min before ischemia, respectively, DM2 group received 50 μg/kg DEX intraperitoneally 30 min after reperfusion, and IR group received normal saline. After 6 h of reperfusion, assessment of liver function, histopathology, oxidative stress was performed. The liver cell microstructure was detected by transmission electron microscopy. Hepatocyte apoptosis was determined by TUNEL assay. Real-time PCR, Western blotting were performed to analyze various ERS molecules. Results: We observed that DEX protected the liver by alleviating hepatocytes damage, reducing the content of ALT and MDA, increasing the activity of SOD, reducing the number of TUNEL-positive cells, down-regulating the expression of GRP-78, PERK, ATF-6, Caspase-12 mRNA, and p-PERK, p-IRE-1 α, CHOP proteins, up-regulating Bcl-2 protein. The effect of 50 μg/kg DEX is superior to 25 μg/kg DEX, but not significantly different from 100μg/kg DEX. There was no significant difference in the above monitoring indexes between DM1 and DM2 group. Conclusions: DEX protects the liver from IRI by inhibiting ERS and cell apoptosis. The protective effect of DEX was dose-dependent in a certain dose range, both DEX administered prior to ischemia and following reperfusion markedly reduced liver injury induced by hepatic IRI in mice.

scholarly journals Extracellular vesicles from bone marrow-derived mesenchymal stem cells protect against murine hepatic ischemia/reperfusion injury

2017 ◽  
Vol 23 (6) ◽  
pp. 791-803 ◽  
Author(s):  
Hiroaki Haga ◽  
Irene K. Yan ◽  
David A. Borrelli ◽  
Akiko Matsuda ◽  
Mansi Parasramka ◽  
...  
Keyword(s):  
Stem Cells ◽  
Bone Marrow ◽  
Mesenchymal Stem Cells ◽  
Reperfusion Injury ◽  
Extracellular Vesicles ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Hepatic Ischemia ◽  
Hepatic Ischemia Reperfusion
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