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Objective:To investigate the clinical application of Bushen-Liyan Decoction combined with low frequency pulse acupoint electrical stimulation in the treatment of swallowing dysfunction of stroke patients in convalescent stage. Methods:From January 2018 to March 2020, 108 stroke patients with swallowing dysfunction in the Shandong Provincial Third Hospital were selected. They were randomly divided into two groups with 54 in each according to the random number table method. The control group was given low frequency pulse acupoint electrical stimulation on the basis of conventional treatment, and the study group was given Bushen-Liyan Decoction combined with low frequency pulse acupoint electrical stimulation on the basis of conventional treatment. Both groups were treated for 4 weeks. The National Institutes of Health Neurological Deficit Score (NIHSS) was used to assess the degree of neurological impairment, the Wada Drinking Water Test was used to assess the degree of swallowing dysfunction, and Barthel Index was used to assess the ability of daily living. The serum levels of brain-derived neurotrophic factor (BDNF), insulin-like growth factor-1 (IGF-1), VEGF, IL-18, IL-23, SOD and MDA were detected by ELISA. The adverse reactions during the treatment were observed and the clinical efficacy was evaluated.Results:The total effective rate was 92.6% (50/54) in the study group and 72.2% (39/54) in the control group, with significant difference between the two groups( χ2=7.728, P=0.005). After treatment, NIHSS score and Wata’s drinking water test score of the study group were lower than those in the control group ( t=8.383, 9.740, P<0.001), Barthel index of the study group was significantly higher than that of the control group ( t=4.064, P<0.01). The serum BDNF [(8.42 ± 0.72) μg/L vs. (6.69 ± 0.63) μg/L, t=13.288], IGF-1[(142.20 ± 12.29) μg/L vs. (118.35 ± 10.73) μg/L, t=10.742] and VEGF[(151.29 ± 12.26) ng/L vs. (102.21 ± 9.77) ng/L, t=23.006] were significantly higher than those in control group( P<0.01); The serum levels of IL-18, IL-23 and MDA were significantly lower than those in the control group( t=7.892, 9.897, 6.206, P<0.001), and the level of SOD was significantly higher than that of the control group ( t=18.510, P<0.001). During the treatment, no serious adverse events occurred in both groups. Conclusion:Bushen-Liyan Decoction combined with low-frequency pulse acupoint electrical stimulation can reduce the clinical symptoms, inflammatory reaction and brain tissue damage of stroke patients with dysphagia, improve the swallowing function and improve the clinical efficacy.
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Objective To investigate effects of ischemic postconditioning on the nitric oxide ( NO) and nitric oxide synthase ( NOS) in diabetic rat brain tissues .Methods Thirty Wistar rats were diabetic models induced by intraperitoneal injuction of stepto-zotocin (STZ), and randomly divided into three groups: Control group (normal, diabetic), cerebral ischemia group, and ischemic postconditioning ( I-POST) group.The rats of cerebral ischemia group and ischemic postconditioning group were made model of cere -bral ischemia by ligation carotid artery .Hematoxylin-eosin ( HE) was used to observe their pathological changes in control and diabetic groups.Enzyme-linked immunosorbent assay ( ELISA) method was used to detect the expression and changes of NO and NOS in the sera in each group .Western Blot method was used to investigate the expression and changes of NOS in the retinal tissues in each group .Results For I-POST group , brain tissue defects were decreased , neuronal cells were increased , serum inducible NOS ( iNOS) content was significantly lower than endothelial NOS (eNOS) and neuronal NOS (nNOS) ( P 0.05 ) .Conclusions Is-chemic postconditioning can protect the brain tissue of diabetic rats by inhibiting NOS activity especially iNOS .
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Objective To evaluate the effects of leg ischemic postconditioning on focal cerebral ischemia-reperfusion (I/R) injury in diabetic rats. Methods Forty male diabetic SD rats weighing 270-320 g were randomly assigned to one of 4 groups (n=10 each):group Ⅰcontrol (C);group Ⅱ sham operation (S);group Ⅲ fecal cerebral ischemia-repertusion (I/R) and group Ⅳ leg ischemic postconditioning (IPC). Diabetes mellitus was induced by intraperitoneal streptozotocin. Local cerebral I/R was produced by middle cerebral artery occlusion (MCAO) for 1.5 h followed by 6 h reperfusion. A nylon thread with rounded tip was inserted into internal carotid artery and threaded cranially until resistance was felt. Leg isebemia was induced by placing tourniquet on beth legs at 30 min before repeffusion. The animals underwent 3 episodes of 5 min leg ischemia at 5 min intervals. Neuro-functional deficit was assessed and recorded at the end of 6h reperfusion using neurologic deficit scores (NDS) (0=no deficit, 4=unable to crawl and semiconscious). The animals were then decapitated and their brains were removed for determination of volume of cerebral infaret (by TIC staining) and ratio' of neuronal apoptosis (by TUNEL). Results NDS and cerebral infarct volume were significantly increased at the end of 6 h reperfusion in group I/R and IPC as compared with group C and S. IPC significantly decreased cerebral infarct volume and ratio of neuronal apoptosis induced by MCAO. There was no significant difference in NDA between group I/R and IPC. Conclusion Leg iscbemic postconditioning can protect the brain against focal cerebral I/R injury in diabetic rats.
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Objective To observe the effect of ischemic postconditioning on cerebral ischemia-reperfusion (I/R)injury in diabetic rats. Methods A rat model of diabetes was established using a single intraperitoneal injection of streptozotocin in 40 male Spragne-Dawley rats.Focal ischemia was induced by transient middle cerebral artery occlusion(MCAO)using a thread.The rats were randomly assigned to a control group,a sham-operated group,an I/R group and an Ⅰ-Post group.The animals in the I/R group were subjected to MCAO for 90 min and then reperfusion.Those in the Ⅰ-post group were subjected to MCAO and 3 cycles of transient ischemia-reperfusion(15 seconds ischemia then 15 seconds reperfusion)before persistent reperfusion.Neurological deficit scores,infarct volume,histological changes in the brain and the number of apoptotic cells were measured 6 hours later.Results There was no significant difference in neurological deficit scores between the I/R group and the Ⅰ-post group.The histological changes and apoptotic cells were significantly less in the Ⅰ-post group compared with the I/R group.Conclusion Ischemic postconditioning can inhibit cell apoptosis and reduce cerebral I/R injury after focal cerebral ischemia-reperfusion in diabetic rats.
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Objective To investigate effects of limbs ischemic postconditioning induced remote postconditioning (RPostC) on mitochondria structure and function after focal cerebral ischemic reperfusion(I/R) injury in diabetic rats. Methods The diabetic rats models were induced by injecting streptozotocin into abdominal cavity. I/R rats models were made by MCAO with thread. Forty male SD rats models were assigned to 4 groups: control group; sham operation group; I/R group;RPostC group ( n=10 ) . 6 h after the reperfusion, the brains were obtained for HE staining. The mitchondria were isolated and content of MDA,the activities of SOD,Na+/K+-ATPase,Ca2+-ATPase and GSH-Px were tested. Morphological changes of neuronal mitochondria were observed by electronic microscope. Results In the I/R group,the content of mitchondria MDA[(4.99?1.25) nmol/mgprot]were markedly increased (P