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

Autor: Weidong Mi, Yun‐Feng Li, You-Zhi Zhang, Zhi‐Peng Xv, Zhen‐Zhen Sun
Rok vydání: 2019
Předmět:
0301 basic medicine
Lipopolysaccharides
Male
Lipopolysaccharide
medicine.medical_treatment
Apoptosis
Smad2 Protein
Biochemistry
chemistry.chemical_compound
Mice
0302 clinical medicine
Transforming Growth Factor beta
Medicine
Postoperative Period
Saline
Neurons
Behavior
Animal
hemic and immune systems
Cell Differentiation
030220 oncology & carcinogenesis
Signal transduction
medicine.symptom
Signal Transduction
medicine.medical_specialty
Cell Survival
Inflammation
Bone Marrow Cells
Enzyme-Linked Immunosorbent Assay
Mesenchymal Stem Cell Transplantation
03 medical and health sciences
stomatognathic system
Internal medicine
Animals
Cognitive Dysfunction
Molecular Biology
Neuroinflammation
business.industry
Mesenchymal Stem Cells
Cell Biology
medicine.disease
Mice
Inbred C57BL
Disease Models
Animal
030104 developmental biology
Endocrinology
chemistry
business
Postoperative cognitive dysfunction
Transforming growth factor
Zdroj: Journal of cellular biochemistry. 121(1)
ISSN: 1097-4644
Popis: 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.
Databáze: OpenAIRE
Externí odkaz: