Background: Exercise preconditioning (EP) is essential for preventing ischemic stroke. Recent studies have shown that EP exerts neuroprotective effects in the cerebral ischemia‐reperfusion injury model. Nonetheless, there have been few reports on the relationship between EP and the Th17/Treg balance. Moreover, it is unclear whether the JAK2/STAT3 pathway is responsible for the neuroprotective effect of EP. Therefore, we aimed to explore the impact of EP, other than the anti‐inflammatory and antiapoptotic functions, on the Th17/Treg balance via the JAK2/STAT3 pathway in a middle cerebral artery occlusion (MCAO)‐induced model.Results: Fifty rats were randomly allocated into five groups, including the sham group (n = 10), EP+sham group (n = 10), MCAO group (n = 10), EP+MCAO group (n = 10), and EP+MCAO+JAK2/STAT3 pathway agonist (coumermycin A1, CA1) group (n = 10). The results indicated that EP alleviated neurological deficits, reduced infarct volume, and ameliorated neuronal apoptosis induced by MCAO. Additionally, the MCAO‐induced Th17/Treg imbalance could be rectified by EP. The decreased levels of IL‐10 and Foxp3 and increased IL‐17 and RORα in the MCAO group were reversed by EP treatment. Regarding inflammation, EP reduced the concentrations of IL‐6 and IL‐17 and elevated those of IL‐10 and TGF‑β. The neuroprotective effects of EP were accompanied by decreased phosphorylation of JAK2 and STAT3. Furthermore, CA1 pretreatment diminished all the beneficial effects of EP partially.Conclusion: Our findings suggest that EP contributes to attenuating neuronal apoptosis, Th17/Treg imbalance, and inflammation induced by MCAO via inhibiting the JAK2/STAT3 pathway, indicating its therapeutic potential in ischemic stroke.

Numerous studies have investigated the relationship between theLRRK2G2385R variant and clinical characteristics in Parkinson’s disease (PD), but the results have been inconsistent. This study investigated whether theLRRK2G2385R variant was associated with a unique clinical phenotype of PD in the Asian population, using a meta-analysis. The PubMed, Web of Science, EMBASE, CNKI, and WANFANG databases were searched until September 2017. The strict selection criteria and exclusion criteria were determined, and mean differences (MD) or odds ratios (OR) with 95% confidence intervals (CI) were used to assess the strength of associations. Statistical analyses and graphics were performed using Review Manager 5.3. Sixteen related case-control studies were included in the meta-analysis. TheLRRK2G2385R carriers significantly more often presented a family history (OR: 1.98; 95% CI: 1.16−3.39;P=0.01) and had a longer disease duration (MD = 0.47, 95% CI: 0.01−0.93,P=0.04) and a higher MMSE score (MD = 1.02, 95% CI: 0.43–1.62P=0.0007) thanLRRK2G2385R noncarriers. There were no significant differences in sex distribution, age at onset, initial symptoms, motor symptoms, depression, levodopa-equivalent dose, and related complications betweenLRRK2G2385R-carrier andLRRK2G2385R-noncarrier PD patients. Our results suggested that most of the clinical characteristics of PD patients withLRRK2G2385R mutations are similar to those ofLRRK2G2385R noncarriers among Asian PD patients, except for the more common family history, relatively longer disease duration, and higher MMSE scores in the former group.