Abstract
This paper aimed to explore the roles of the combination of electroacupuncture (EA) and induced pluripotent stem cell-derived small extracellular vesicles (iPSC-EVs) on mice with ischemic stroke and the underlying mechanisms. A focal cerebral ischemia model was established in C57BL/6 mice through middle cerebral artery occlusion (MCAO). After 3 days, neurological impairment and motor function were examined by performing behavioral tests. The infarct volume and neuronal apoptosis were examined using TTC staining and TUNEL assays. Flow cytometry was performed to assess the proliferation of T lymphocytes. The changes in the interleukin (IL)-33/ST2 axis were evaluated by immunofluorescence and Western blotting. The combination of EA and iPSC-EVs treatment ameliorated neurological impairments and reduced the infarct volume and neuronal apoptosis in MCAO mice. EA plus iPSC-EVs suppressed T helper (Th1) and Th17 responses and promoted the regulatory T cell (Treg) response. In addition, EA plus iPSC-EVs exerted neuroprotective effects by regulating the IL-33/ST2 axis and inhibiting the microglia and astrocyte activation. Taken together, the study shows that EA and iPSC-EVs exerted a synergistic neuroprotective effect in MCAO mice, and this treatment may represent a novel potent therapy for ischemic stroke and damage to other tissues.
Highlights
IntroductionA common neurological disorder, leads to permanent disability in patients worldwide [1–3]
Ischemic stroke, a common neurological disorder, leads to permanent disability in patients worldwide [1–3]
We used a middle cerebral artery occlusion (MCAO) mouse model to determine the effects of EA and Induced pluripotent stem cells (iPSCs)-EVs on the motor function of mice with ischemic stroke
Summary
A common neurological disorder, leads to permanent disability in patients worldwide [1–3]. Neuroinflammation induced by ischemic stroke plays an essential role in multiple mechanisms leading to secondary brain injury after stroke [4]. T lymphocytes are key mediators of neuroinflammation induced by ischemic stroke [11]. T helper 1 cells (Th1) promote inflammation, and Th2 cells preferentially induce antiinflammatory responses [12]. A previous study showed a significant increment of Th17 cells and a marked reduction of peripheral regulatory T (Treg) cells in ischemic stroke patients, suggesting that the peripheral Th17/Treg imbalance might underlie the pathogenesis of ischemic stroke [13]. Recent studies have reported an upregulation of Treg cell numbers in the mice brain, and these cells may promote functional recovery and brain repair following stroke [14,15]. A deeper study of the effects of T lymphocytes is imperative for ischemic stroke therapy
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