ABSTRACT
As an important tool to evaluate cardiac autonomic function, heart rate variability (HRV) is closely associated with ischemic stroke. The change of HRV can not only increase the incidence and recurrence risk of ischemic stroke, but also affect the severity of the disease and the risk of complications, resulting in poor outcomes. Effective intervention for patients with stroke to restore their autonomic nerve function is expected to become a new target for the treatment of ischemic stroke. This article reviews the research progress of the correlation between HRV changes and ischemic stroke.
ABSTRACT
Objective To investigate the role of phosphatidyl inositol 3 kinase (PI3K)/Akt pathway in the protection of focal cerebral ischemia reperfusion injury in rats with limb ischemic postconditioning (LIP) by detecting the expression levels of p-Akt protein, and caspase-9 and Bcl-2 mRNAs after remote LIP. Methods Forty-two Wistar rats were randomly assigned to 3 groups: sham operation, ischemia-reperfusion (IR) and LIP groups. The middle cerebral artery ischemia-reperfusion injury model was induced by the suture method in the IR group and the LIP group. In the LIP group, three circulatory LIP ( 5 min ischemia/5 min reperfusion) in the contralateral femoral artery were performed before reperfusion 2 h after cerebral ischemia. Infarct volume was measured by 2,3,5-triphenyltetrazolium chloride staining. The expression of p-Akt protein was detected by immunohistochemical staining and the expression levels of cystin-9 and Bcl-2 mRNAs were detected by in situ hybridization. Results Compared with the IR group, the infarct volume in the LIP group was significantly reduced ( P<0.05). The expression levels of p-Akt protein and Bcl-2 mRNA significantly increased (all P<0.05), and the expression level of caspase-9 mRNA significantly decreased (P<0.05). Conclusions LIP can reduce the volume of cerebral infarction in focal cerebral ischemia-reperfusion injury in rats. Its mechanism may be involved in up-regulation of p-Akt protein and Bcl-2 mRNA expression and down-regulation of caspase-9 mRNA expression, suggesting that LIP can alleviate cerebral ischemia-reperfusion injury through PI3K/Akt pathway.
ABSTRACT
Glycemic variability is closely related to diabetes complications,and might play a more valuable role in clinical risk assessment.The glycemic variability could effect the prognosis of cardiovascular disease and ischemic stroke.Meanwhile,it has a close relationship with the presence, development and severity of diabetic nephropathy.Moreover,as an independent risk factor for the damage of macro- and microvessels,it has a positive relationship with the severity of target organ.Therefore,the strategy to regulate glycemic variability is a valuable measure of glycemic control,and may be of great significance to strengthen the effect of diabetes treatment and reduce the damage on target organs.
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ObjectiveToinvestigatetherolesofbrain-derivedneurotrophicfactor(BDNF)and tyrosine receptor kinase B (TrkB) in ischemic postconditioning. Methods Wistar rats w ere randomly assigned to three groups:a sham operation (9 rats), an ischemic postconditioning, and an ischemia-reperfusion group. According to the reperfusion time, the latter 2 groups w ere redivided into 6, 12, 24, 48, and 72 h subgroups (9 rats in each subgroups). A middle cerebral artery occluded by suture method for a cerebral ischemia-reperfusion model. Triphenyl tetrazolium staining w as used to detect infarct volume (P=4). Immunohisto-chemical staining w as used to detect the expression levels of BDNF and TrkB proteins (P=5). Results The infarct volumes in the ischemic postconditioning group w ere reduced significantly compared w ith those in the ischemia-reperfusion group (6 h:143.3 ±8.7 mm3 vs.166.8 ±7.5 mm3, t=4.104, P=0.006;12 h:151.7 ±7.8 mm3 vs.171.6 ±9.1 mm3, t=3.314, P=0.016; 24 h: 159.2 ±9.3 mm3 vs.177.1 ± 7.6 mm3, t=3.000, P=0.024;48 h:166.9 ±9.6 mm3 vs.184.9 ±9.0 mm3, t=2.732, P=0.034;72 h:172.0 ±9.1 mm3 vs.198.1 ±8.2 mm3, t=2.640, P=0.039), and the positive cel numbers of BDNF (6 h:23.98 ±4.07 vs.18.63 ±2.5, t=2.479, P=0.038;12 h:27.64 ±3.18 vs.22.01 ±3.14, t=2.817, P=0.023;24 h:34.82 ±4.17 vs.28.46 ±4.05, t=2.446, P=0.040; 48 h:34.30 ±3.27 vs.26.29 ± 3.26, t=3.872, P=0.005;72 h:28.77 ±3.53 vs.23.64 ±3.54, t=2.297, P=0.051) and TrkB (6 h:33.83 ±3.90 vs.21.51 ±3.86, t=5.012, P<0.001; 12 h:38.59 ±4.84 vs.23.41 ±3.67, t=5.586, P<0.001;24 h:46.07 ±3.06 vs.28.78 ±3.61, t=8.169, P<0.001; 48 h:47.90 ±3.30 vs.29.51 ± 3.81, t=8.160, P<0.001; 72 h:42.78 ±4.07 vs.27.46 ±3.19, t=6.623, P<0.001) per high-pow er field at each time point in the ischemic postconditioning group w ere significantly more than those in the ischemia-reperfusion group. Conclusions Ischemic postconditioning upregulates the expressions levels of BDNF and TrkB proteins after ischemia-reperfusion and reduces cerebral infarct volumes. BDNF/TrkB may play an important neuroprotective effect in ischemic postconditioning.
ABSTRACT
Objective To investigate the effect of cerebral ischemic preconditioning (IP) on the expressions of angiopoietin-1 (Ang-1) and its receptor Tie-2 mRNA in cerebral ischemia in rats.Methods Ninety-nine Wistar rats were randomly assigned to three groups:sham operation (n =9),non-ischemic preconditioning (NIP) (n =45),and IP (n =45).The latter two groups were redivided into 5 subgroups:ischemia-reperfusion 1,3,7,14,and 21 days (n =9 in each group).A model of transient middle cerebral artery occlusion (MCAO) was induced by the intraluminal suture method for focal IP (ischemia for 10 minutes and restoring perfusion).Infarct volume was determined by 2,3,5-triphenyltetrazolium staining.The expression levels of Ang-1/Tie-2 mRNA were detected by in situ hybridization.Results The infarct volumes in the 1 -,3-,and 7-day subgroups of the IP group were significantly smaller than those in the relative subgroups of the NIP group (all P＜ 0.05).The expression of Ang-1 mRNA in the 3- and 7-day subgroups of the IP group and the expression of Tie-2 mRNA in the 1-,3-,and 7-day subgroups of the NIP group were upregulated significantly (all P ＜ 0.05).The infarct volume in the 3-day subgroup of the IP group was reduced most significantly (P ＜ 0.05).The expression of Ang-1 mRNA in the 7-day subgroup was upregulated significantly,and the peak expression of its receptor Tie-2 mRNA appeared at day 3 after IP and continued to day 7.Pearson correlation analysis showed that the expression levels of Ang-1/Tie-2 mRNA were significantly negatively correlated with infarct volume (P ＜0.01).Conclusions The expression of Ang-1/Tie-2 mRNA in the IP group was upregulated within the time window of ischemic tolerance (1 - 7 days after preconditioning),in which Ang-1 may mainly act on the later stage of the cerebral ischemic tolerance.