Bone marrow mesenchymal stem cells regulate TGF‐β to adjust neuroinflammation in postoperative central inflammatory mice

Background Postoperative cognitive dysfunction (POCD) is one of the common postoperative complications, which is more common in aged patients. POCD mainly manifests as cognitive function changes after surgery, such as memory decline and inattention. In some severe cases, patients may suffer from per...

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Veröffentlicht in:Journal of cellular biochemistry Jg. 121; H. 1; S. 371 - 384
Hauptverfasser: Sun, Zhen‐Zhen, Li, Yun‐Feng, Xv, Zhi‐Peng, Zhang, You‐Zhi, Mi, Wei‐Dong
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Veröffentlicht: United States Wiley Subscription Services, Inc 01.01.2020
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Abstract Background Postoperative cognitive dysfunction (POCD) is one of the common postoperative complications, which is more common in aged patients. POCD mainly manifests as cognitive function changes after surgery, such as memory decline and inattention. In some severe cases, patients may suffer from personality changes and (or) social behavior decline. The aim of the current study is to confirm the effect and elucidate the mechanism of bone marrow mesenchymal stem cells (BMSCs) in postoperative central inflammatory mice. Methods Mice were randomly assigned to four groups: sham, sham+BMSCs, model, and BMSCs group. In the model group, mice were intraperitoneally injected 8 mg/kg per day lipopolysaccharide for 5 days. In sham+BMSCs and BMSCs group, BMSCs (1 × 10 7) in 100 µL saline were injected into sham mice and model mice, respectively. Results In the model group, transforming growth factor β (TGF‐β) protein expression was significantly increased, compared with that in the sham group. BMSCs were treated into postoperative central inflammatory mice, which resulted in a decreased of TGF‐β protein expression. TGF‐β and smad2 protein expression were suppressed, and apoptosis rate and inflammation were inhibited in coculture with BMSCs. The suppression of TGF‐β inhibited the effects of BMSCs on apoptosis rate and inflammation in postoperative central inflammatory through a smad2 signaling pathway. The promotion of TGF‐β reduced the effects of BMSCs on apoptosis rate and inflammation in postoperative central inflammatory through a smad2 signaling pathway. Conclusion The present study demonstrates that BMSCs regulates TGF‐β to adjust neuroinflammation in postoperative central inflammatory mice.
AbstractList BackgroundPostoperative cognitive dysfunction (POCD) is one of the common postoperative complications, which is more common in aged patients. POCD mainly manifests as cognitive function changes after surgery, such as memory decline and inattention. In some severe cases, patients may suffer from personality changes and (or) social behavior decline. The aim of the current study is to confirm the effect and elucidate the mechanism of bone marrow mesenchymal stem cells (BMSCs) in postoperative central inflammatory mice.MethodsMice were randomly assigned to four groups: sham, sham+BMSCs, model, and BMSCs group. In the model group, mice were intraperitoneally injected 8 mg/kg per day lipopolysaccharide for 5 days. In sham+BMSCs and BMSCs group, BMSCs (1 × 107) in 100 µL saline were injected into sham mice and model mice, respectively.ResultsIn the model group, transforming growth factor β (TGF‐β) protein expression was significantly increased, compared with that in the sham group. BMSCs were treated into postoperative central inflammatory mice, which resulted in a decreased of TGF‐β protein expression. TGF‐β and smad2 protein expression were suppressed, and apoptosis rate and inflammation were inhibited in coculture with BMSCs. The suppression of TGF‐β inhibited the effects of BMSCs on apoptosis rate and inflammation in postoperative central inflammatory through a smad2 signaling pathway. The promotion of TGF‐β reduced the effects of BMSCs on apoptosis rate and inflammation in postoperative central inflammatory through a smad2 signaling pathway.ConclusionThe present study demonstrates that BMSCs regulates TGF‐β to adjust neuroinflammation in postoperative central inflammatory mice.
Postoperative cognitive dysfunction (POCD) is one of the common postoperative complications, which is more common in aged patients. POCD mainly manifests as cognitive function changes after surgery, such as memory decline and inattention. In some severe cases, patients may suffer from personality changes and (or) social behavior decline. The aim of the current study is to confirm the effect and elucidate the mechanism of bone marrow mesenchymal stem cells (BMSCs) in postoperative central inflammatory mice. Mice were randomly assigned to four groups: sham, sham+BMSCs, model, and BMSCs group. In the model group, mice were intraperitoneally injected 8 mg/kg per day lipopolysaccharide for 5 days. In sham+BMSCs and BMSCs group, BMSCs (1 × 10 ) in 100 µL saline were injected into sham mice and model mice, respectively. In the model group, transforming growth factor β (TGF-β) protein expression was significantly increased, compared with that in the sham group. BMSCs were treated into postoperative central inflammatory mice, which resulted in a decreased of TGF-β protein expression. TGF-β and smad2 protein expression were suppressed, and apoptosis rate and inflammation were inhibited in coculture with BMSCs. The suppression of TGF-β inhibited the effects of BMSCs on apoptosis rate and inflammation in postoperative central inflammatory through a smad2 signaling pathway. The promotion of TGF-β reduced the effects of BMSCs on apoptosis rate and inflammation in postoperative central inflammatory through a smad2 signaling pathway. The present study demonstrates that BMSCs regulates TGF-β to adjust neuroinflammation in postoperative central inflammatory mice.
Background Postoperative cognitive dysfunction (POCD) is one of the common postoperative complications, which is more common in aged patients. POCD mainly manifests as cognitive function changes after surgery, such as memory decline and inattention. In some severe cases, patients may suffer from personality changes and (or) social behavior decline. The aim of the current study is to confirm the effect and elucidate the mechanism of bone marrow mesenchymal stem cells (BMSCs) in postoperative central inflammatory mice. Methods Mice were randomly assigned to four groups: sham, sham+BMSCs, model, and BMSCs group. In the model group, mice were intraperitoneally injected 8 mg/kg per day lipopolysaccharide for 5 days. In sham+BMSCs and BMSCs group, BMSCs (1 × 10 7) in 100 µL saline were injected into sham mice and model mice, respectively. Results In the model group, transforming growth factor β (TGF‐β) protein expression was significantly increased, compared with that in the sham group. BMSCs were treated into postoperative central inflammatory mice, which resulted in a decreased of TGF‐β protein expression. TGF‐β and smad2 protein expression were suppressed, and apoptosis rate and inflammation were inhibited in coculture with BMSCs. The suppression of TGF‐β inhibited the effects of BMSCs on apoptosis rate and inflammation in postoperative central inflammatory through a smad2 signaling pathway. The promotion of TGF‐β reduced the effects of BMSCs on apoptosis rate and inflammation in postoperative central inflammatory through a smad2 signaling pathway. Conclusion The present study demonstrates that BMSCs regulates TGF‐β to adjust neuroinflammation in postoperative central inflammatory mice.
Postoperative cognitive dysfunction (POCD) is one of the common postoperative complications, which is more common in aged patients. POCD mainly manifests as cognitive function changes after surgery, such as memory decline and inattention. In some severe cases, patients may suffer from personality changes and (or) social behavior decline. The aim of the current study is to confirm the effect and elucidate the mechanism of bone marrow mesenchymal stem cells (BMSCs) in postoperative central inflammatory mice.BACKGROUNDPostoperative cognitive dysfunction (POCD) is one of the common postoperative complications, which is more common in aged patients. POCD mainly manifests as cognitive function changes after surgery, such as memory decline and inattention. In some severe cases, patients may suffer from personality changes and (or) social behavior decline. The aim of the current study is to confirm the effect and elucidate the mechanism of bone marrow mesenchymal stem cells (BMSCs) in postoperative central inflammatory mice.Mice were randomly assigned to four groups: sham, sham+BMSCs, model, and BMSCs group. In the model group, mice were intraperitoneally injected 8 mg/kg per day lipopolysaccharide for 5 days. In sham+BMSCs and BMSCs group, BMSCs (1 × 10 7 ) in 100 µL saline were injected into sham mice and model mice, respectively.METHODSMice were randomly assigned to four groups: sham, sham+BMSCs, model, and BMSCs group. In the model group, mice were intraperitoneally injected 8 mg/kg per day lipopolysaccharide for 5 days. In sham+BMSCs and BMSCs group, BMSCs (1 × 10 7 ) in 100 µL saline were injected into sham mice and model mice, respectively.In the model group, transforming growth factor β (TGF-β) protein expression was significantly increased, compared with that in the sham group. BMSCs were treated into postoperative central inflammatory mice, which resulted in a decreased of TGF-β protein expression. TGF-β and smad2 protein expression were suppressed, and apoptosis rate and inflammation were inhibited in coculture with BMSCs. The suppression of TGF-β inhibited the effects of BMSCs on apoptosis rate and inflammation in postoperative central inflammatory through a smad2 signaling pathway. The promotion of TGF-β reduced the effects of BMSCs on apoptosis rate and inflammation in postoperative central inflammatory through a smad2 signaling pathway.RESULTSIn the model group, transforming growth factor β (TGF-β) protein expression was significantly increased, compared with that in the sham group. BMSCs were treated into postoperative central inflammatory mice, which resulted in a decreased of TGF-β protein expression. TGF-β and smad2 protein expression were suppressed, and apoptosis rate and inflammation were inhibited in coculture with BMSCs. The suppression of TGF-β inhibited the effects of BMSCs on apoptosis rate and inflammation in postoperative central inflammatory through a smad2 signaling pathway. The promotion of TGF-β reduced the effects of BMSCs on apoptosis rate and inflammation in postoperative central inflammatory through a smad2 signaling pathway.The present study demonstrates that BMSCs regulates TGF-β to adjust neuroinflammation in postoperative central inflammatory mice.CONCLUSIONThe present study demonstrates that BMSCs regulates TGF-β to adjust neuroinflammation in postoperative central inflammatory mice.
Author Xv, Zhi‐Peng
Sun, Zhen‐Zhen
Zhang, You‐Zhi
Mi, Wei‐Dong
Li, Yun‐Feng
Author_xml – sequence: 1
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  organization: Shenzhen University General Hospital & Shenzhen University Clinical Medical Academy
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  givenname: Yun‐Feng
  surname: Li
  fullname: Li, Yun‐Feng
  organization: Beijing Institute of Pharmacology and Toxicology
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  fullname: Xv, Zhi‐Peng
  organization: Chinese PLA General Hospital
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  givenname: Wei‐Dong
  orcidid: 0000-0002-5606-6450
  surname: Mi
  fullname: Mi, Wei‐Dong
  email: weidong_mi@aliyun.com
  organization: Chinese PLA General Hospital
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Keywords TGF-β
postoperative central inflammatory
neuroinflammation
BMSCs
Language English
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Snippet Background Postoperative cognitive dysfunction (POCD) is one of the common postoperative complications, which is more common in aged patients. POCD mainly...
Postoperative cognitive dysfunction (POCD) is one of the common postoperative complications, which is more common in aged patients. POCD mainly manifests as...
BackgroundPostoperative cognitive dysfunction (POCD) is one of the common postoperative complications, which is more common in aged patients. POCD mainly...
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SubjectTerms Animal models
Animals
Apoptosis
Behavior, Animal
BMSCs
Bone marrow
Bone Marrow Cells - metabolism
Cell Differentiation - drug effects
Cell Survival
Cognitive ability
Cognitive Dysfunction - metabolism
Disease Models, Animal
Enzyme-Linked Immunosorbent Assay
Growth factors
Inflammation
Inflammation - metabolism
Inhibition (psychology)
Lipopolysaccharides
Lipopolysaccharides - metabolism
Male
Mesenchymal Stem Cell Transplantation
Mesenchymal stem cells
Mesenchymal Stem Cells - cytology
Mesenchyme
Mice
Mice, Inbred C57BL
neuroinflammation
Neurons - metabolism
postoperative central inflammatory
Postoperative Period
Protein expression
Proteins
Signal Transduction
Signaling
Smad2 protein
Smad2 Protein - metabolism
Social behavior
Stem cell transplantation
Stem cells
Surgery
TGF‐β
Transforming Growth Factor beta - metabolism
Transforming growth factor-b
Title Bone marrow mesenchymal stem cells regulate TGF‐β to adjust neuroinflammation in postoperative central inflammatory mice
URI https://onlinelibrary.wiley.com/doi/abs/10.1002%2Fjcb.29188
https://www.ncbi.nlm.nih.gov/pubmed/31218737
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Volume 121
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