Abstract
Acute ischemic stroke (AIS) generally causes neurological dysfunction and poses a serious threat to public health. Here, we aimed to assess the independent and combined effects of ginsenoside Rb1 (GRb1) and Emodin on neuroprotection through regulating Connexin 43 (Cx43) and Aquaporin 4 (AQP4) expression in cerebral ischemia/reperfusion (I/R) model rats. Adult male Sprague-Dawley (SD) rats were randomly divided into five groups: sham group, I/R group, Emodin group, GRb1 group and Emodin+GRb1 group. They were further allocated to four subgroups according to the 6h, 1d, 3d, and 7d time points except the sham group. Based on the modified Longa suture method, the focal cerebral I/R model was established by middle cerebral artery occlusion (MCAO). The neurological deficit scores (NDS), blood brain barrier (BBB) permeability and cerebral infarction area were assessed at each corresponding time point. Cx43 and AQP4 levels were assessed by Real-time PCR and Immunofluorescence. Compared with I/R group, both the independent and combined use of GRb1 and Emodin could alleviate NDS, reduce the BBB permeability, reduce the infarction area and down-regulate Cx43 and AQP4 expression at 6h, 1d, 3d, and 7d after I/R (P < 0.05). The Emodin+GRb1 group had more significant effects than Emodin group and GRb1 group (P < 0.05). In conclusion, the combination of Emodin and GRb1 exerts synergistically neuroprotective functions through regulating AQP4 and Cx43 after I/R.
Highlights
Acute ischemic stroke (AIS) generally causes vascular occlusions and cerebral blood flow blocked, brain ischemia and hypoxia, and necrosis of brain tissue, which results in neurological dysfunction (Bangalore et al, 2014), accounting for approximately 87% of strokes (Mozaffarian et al, 2016)
Cerebral infarction resulted in neurological function deficit in the rats, which was mainly detected as contralateral forelimb paralysis
One-way analysis of variance (ANOVA) showed a significantly difference among Sham group, I/R group, ginsenoside Rb1 (GRb1) group, Emodin group and GRb1+Emodin group in neurological deficit scores (NDS) at 6 h (F = 56.52, df = 4, P < 0.0001), 1d (F = 67.07, df = 4, P < 0.0001), 3d (F = 49.78, df = 4, P < 0.0001), and 7d (F = 27.22, df = 4, P < 0.0001)
Summary
Acute ischemic stroke (AIS) generally causes vascular occlusions and cerebral blood flow blocked, brain ischemia and hypoxia, and necrosis of brain tissue, which results in neurological dysfunction (Bangalore et al, 2014), accounting for approximately 87% of strokes (Mozaffarian et al, 2016). According to the 2018 guideline from the American Heart Association/American Stroke Association (AHA/ASA), intravenous thrombolysis of recombinant tissue type plasminogen activator (rtPA) and/or mechanical thrombectomy are two effective treatments for AIS patients (Powers et al, 2018). As for mechanical thrombolysis, the requirements of rapid cerebral angiography in experienced stroke centers and qualified neurointerventional physicians largely impose restrictions on its clinical use (Moussaddy et al, 2018). It is necessary to seek alternative therapeutic approaches for AIS patients
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