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Background/Aims: Ischemic stroke is the main cause of nerve damage and brain dysfunction, accompanied by strong brain cell apoptosis. This study aimed to investigate the effect of kaempferol-3-O-rhamnoside (K-3-rh) on cerebral ischemia-reperfusion (I/R) injury. Methods and Materials: A rat model of cerebral I/R injury was established. The effects of K-3-rh on cerebral infarction size, brain water content and neurological deficits in rats were evaluated. Apoptosis of ischemic brain cells after mouse I/R was observed by TUNEL staining and flow cytometry. Western blot and qRT-PCR were used to detect the effect of K-3-rh on the expression of apoptosis-related proteins. Results: K-3-rh can improve the neurological deficit score, reduce the infarct volume and brain water content, and inhibit cell apoptosis. In addition, K-3-rh significantly downregulated the expression of Bax and p53 and upregulated the expression of Bcl-2, and the phosphorylation level of Akt. Blockade of PI3K activity by the PI3K inhibitor wortmannin not only reversed the effects of K-3-rh on infarct volume and brain water content but also reversed the expression level of p-Akt. Conclusion: K-3-rh had obvious neuroprotective effects on brain I/R injury and neuronal apoptosis, and its mechanism may be related to activation of PI3K/Akt signaling pathway.

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IntroductionRepetitive transcranial magnetic stimulation (rTMS) is an effective non-invasive cortical stimulation technique in the treatment of neuropathic pain. As a new rTMS technique, intermittent theta burst stimulation (iTBS) is also effective at relieving pain. We aimed to establish the pain-relieving effectiveness of different modalities on neuropathic pain. The study was conducted in individuals with spinal cord injury (SCI) and different modalities of rTMS.MethodsThirty-seven individuals with SCI were randomly allocated to three groups, in which the “iTBS” group received iTBS, the “rTMS” group received 10 Hz rTMS, and the “iTBS + rTMS” group received iTBS and 10 Hz rTMS successively of the primary motor cortex 5 days a week for 4 weeks, and they all underwent the full procedures. The primary outcome measure was change in the visual analog scale (VAS), and the secondary outcomes were measured using the Hamilton Rating Scale for Depression (HAM-D) and the Pittsburgh Sleep Quality Index (PSQI). All the outcomes were evaluated at 1 day before stimulation (baseline), 1 day after the first week of stimulation (S1), and 1 day after the last stimulation (S2).ResultsThe VAS scores showed significant pain improvement after 4 weeks of stimulation (p = 0.0396, p = 0.0396, and p = 0.0309, respectively) but not after 1 week of stimulation. HAM-D scores declined, but the decreases were not significant until 4 weeks later (p = 0.0444, p = 0.0315, and p = 0.0447, respectively). PSQI scores were also significantly decreased after 4 weeks of stimulation (p = 0.0446, p = 0.0244, and p = 0.0088, respectively). Comparing the three modalities, VAS, HAM-D, and PSQI scores at S1 showed no differences, and, at S2, VAS scores showed significant differences (p = 0.0120; multiple comparisons showed significant differences between iTBS and iTBS + rTMS, p = 0.0091), while the HAM-D and PSQI scores showed no differences.DiscussionThe primary and secondary outcomes all showed significant improvement, indicating that the three different modalities were all effective at relieving the pain. However, not all the three stimulations were of same effectiveness after treatment; there were statistical differences in the treatment of neuropathic pain between iTBS as a priming stimulus and as a single procedure.