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

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.

The Ferroptosis Inhibitor Liproxstatin-1 Ameliorates LPS-Induced Cognitive Impairment in Mice

“…Massive evidence showed that major surgeries could induce a widespread systemic inflammatory response, and multiple biomarkers of neuro-inflammatory response were widely observed to have an association to the pathophysiological changes underpinning POCD and cognitive deficits in clinical studies [ 4 , 5 ]. This conclusion was verified in multiple surgery rodent models in terms of its mechanism, showing that the upregulation of pro-inflammatory cytokines and inflammatory mediators in the central nervous system (CNS) could cause obvious cognitive impairment in animals, and that it could be blocked by anti-inflammatory agents [ 6 , 7 , 8 ]. Inflammation leads to oxidative stress, contributes to mitochondrial dysfunction [ 9 , 10 , 11 , 12 ], and induces a variety of metabolic disorders, such as iron metabolism disorders.…”