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Objective:To discuss clinical effect of Shexiang Tongxin pills to syndrome of Qi deficiency and blood stasis in ischemic heart failure （IHF） and to study the mechanism to myocardial fibrosis and vascular regeneration. Method:One hundred and forty patients were randomly divided into observation group （70 cases） and control group （70 cases） with the same cases. 66 patients in control group finish the therapy （3 patients fall off or lost visit， 1 were eliminated）. 65 patients in observation group completed the therapy （4 patients were falling off， 1 were eliminated）. Both groups patients got combined treatment according to the guiding. Patients in control group got simulated medicine of Shexiang Tongxin pills， 2 pills/time， 3 times/day. Patients in observation group got Shexiang Tongxin pills， 2 pills/time， 3 times/day. The treatment was continued for 24 weeks. Before and after treatment， the left ventricular ejection fraction （LVEF）， cardiac output （CO）， end diastolic diameter （LVEDd）， left posterior wall thickness （LVPW）， left ventricular mass index （LVMI） and left ventricular remodeling index （LVRI） were measured by echocardiography. And scores of six minute walking test （6 MWT）， Lee's heart failure score， Qi deficiency and blood stasis syndrome score and Minnesota Heart Failure Quality of life questionnaire （MLHFQ） were graded. And levels of N-terminal B-type natriuretic peptide （NT-proBNP）， transforming growth factor-β1 （TGF-β1）， soluble ST2 （sST2）， matrix metalloproteinase-2 （MMP-2）， matrix metalloproteinase inhibitor-2 （TIMP-2）， insulin-like growth factor-1 （IGF-1）， vascular endothelial growth factor （VEGF）， angiopoietin1 （Ang1） and angiopoietin2 （Ang2）， and the safety was evaluated. Result:The total clinical effect in observation group was 90.77% （59/65） higher than 74.24% （49/66） in control group （χ2=6.179， P<0.05）. Levels of LVEF， CO， LVRI， 6 MWT， TIMP-2， IGF-1， VEGF and Ang1 were higher than those in control group （P<0.01）. And levels of LVEDd， LVPW and LVMI were lower than those in control group （P<0.05）， levels of NT-proBNP， TGF-β1， sST2， MMP-2 and Ang2 were lower than those in control group （P<0.01）， scores of Lee's heart failure score， Qi deficiency and blood stasis syndrome score and MLHFQ were lower than those in control group （P<0.01）. Besides， there was no adverse reactions caused by Shexiang Tongxin dropping pills. Conclusion:On the basis of conventional western medicine treatment， Shexiang Tongxin drop pills can improve the ventricular remodeling， improve the heart function， reduce the clinical symptoms， increase the exercise tolerance and quality of life of the patients by affecting the myocardial fibrosis and vascular regeneration factor， which has better clinical efficacy and safety.
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BACKGROUND: In recent years, with the deepening of medical research, it has been found that PI3K/AKT signaling pathway has a regulatory effect on vascular repair regeneration, osteoblast differentiation and proliferation, and osteoclast bone differentiation. This is very important for the treatment of femoral head necrosis. OBJECTIVE: To provide a brief overview of the main research progress in mechanisms of PI3K/AKT signaling pathway regulating femoral head necrosis in recent years, aiming to provide new ideas for the treatment of osteonecrosis of the femoral head in the future. METHODS: PubMed and MEDLINE database, Wanfang, CNKI, WIPO and CBM database were searched from 2012 to 2019, for relevant domestic and foreign literatures, including: (1) epidemiological study of osteonecrosis of the femoral head and related pathogenesis; (2) PI3K/AKT pathway related mechanism; (3) research literature on the effects of PI3K/AKT on factors related to vascular repair and regeneration; (4) research literature on the regulation of PI3K/AKT on osteoblast differentiation and proliferation-related factors; (5) literature on the regulation of PI3K/AKT on functional factors related to osteoclast differentiation. A total of 62 literatures were included for analysis and summary. RESULTS AND CONCLUSION: (1) The PI3K/AKT signaling pathway has been proven to be effective in the regulation of vascular repair regeneration, osteoblast differentiation, proliferation, apoptosis and osteoclast differentiation. After understanding these pathways, research and development of related drugs to improve the success rate of early conservative treatment of osteonecrosis of the femoral head have great development prospects and potential, opening up a new path for future orthopedic surgeons to treat osteonecrosis of the femoral head, and bringing new hope to patients and their families. (2) According to the different osteonecrosis of the femoral head conditions of patients, how to use PI3K/AKT signaling pathway to guide treatment becomes a breakthrough point and challenge of this technology, and more research is needed later.
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Objective: To investigate the impact of cathepsins S (CatS) on aortic ring-derived micro vascular cavity formation in experimental mice. Methods: Hindlimb ischemia model was established in CatS+/+ and CatS-/- mice, n=8 in each group. The blood flow in hindlimb was measured before ischemic surgery; immediately and 1, 4, 7, 14, 21 days after surgery. CatS+/+mice were further divided into 4 subgroups: Normal control subgroup, Selective CatS inhibitor (LHVS) subgroup, Non-selective CatS inhibitor (E64d) subgroup and MMP inhibitor (GM6001) subgroup; n=2 in each subgroup. The mice aortic ring-derived micro vascular cavity formation was observed by FITC-CD31 immunofluorescence method. Results: ① CatS-/- mice had inhibited blood flow recovery after ischemic surgery. Laser Doppler blood flow (LDBF) examination indicated that compared with CatS+/+group, CatS-/- group had slower hindlimb blood flow recovery, P<0.05;② CatS-/-group had the less aortic ring-derived micro vascular cavities, P<0.001. ③ Compared with Normal control subgroup, LHVS subgroup, E64d subgroup and GM6001 subgroup had suppressed micro vascular cavity formation, all P<0.05.④ Aortic ring-derived micro vascular cavity was composed by endothelial cells. Conclusion: CatS plays a beneficial role in ischemic vascular regeneration in experimental mice; it is not only increasing aortic ring-derived micro vascular cavity formation, but also promoting blood flow recovery in ischemic hindlimb. Our finding provides a theoretical basis for new therapeutic target in ischemic vascular regeneration.
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Objective: To investigate the impact of cathepsins S (CatS) on aortic ring-derived micro vascular cavity formation in experimental mice. Methods: Hindlimb ischemia model was established in CatS+/+ and CatS-/- mice, n=8 in each group. The blood flow in hindlimb was measured before ischemic surgery; immediately and 1, 4, 7, 14, 21 days after surgery. CatS+/+mice were further divided into 4 subgroups: Normal control subgroup, Selective CatS inhibitor (LHVS) subgroup, Non-selective CatS inhibitor (E64d) subgroup and MMP inhibitor (GM6001) subgroup; n=2 in each subgroup. The mice aortic ring-derived micro vascular cavity formation was observed by FITC-CD31 immunofluorescence method. Results: ① CatS-/- mice had inhibited blood flow recovery after ischemic surgery. Laser Doppler blood flow (LDBF) examination indicated that compared with CatS+/+group, CatS-/- group had slower hindlimb blood flow recovery, P<0.05;② CatS-/-group had the less aortic ring-derived micro vascular cavities, P<0.001. ③ Compared with Normal control subgroup, LHVS subgroup, E64d subgroup and GM6001 subgroup had suppressed micro vascular cavity formation, all P<0.05.④ Aortic ring-derived micro vascular cavity was composed by endothelial cells. Conclusion: CatS plays a beneficial role in ischemic vascular regeneration in experimental mice; it is not only increasing aortic ring-derived micro vascular cavity formation, but also promoting blood flow recovery in ischemic hindlimb. Our finding provides a theoretical basis for new therapeutic target in ischemic vascular regeneration.
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@#Objective To investigate the change of serum vascular endothelial growth factor (VEGF) in cerebral infarction before and af-ter rehabilitation. Methods Forty-eight patients with first cerebral infarction were enrolled from June, 2014 to August, 2016 in Beijing Bo'ai Hospital. Level of serum VEGF was measured by enzyme-linked immunosorbent assay (ELISA) before and six weeks after rehabilitation. The level of serum VEGF of 33 normal subjects was compared with the patients'. Results The level of serum VEGF was higher in the pa-tients group than in the control group before and six weeks after rehabilitation (t>2.540, P<0.05). The level of VEGF was higher in the large area infarction group (>4 cm) than in the small area infarction group (≤4 cm) (t=4.436, P<0.05), and was higher in the short course (less than one month) infarction group than in the long course (more than one month) group (t=2.316, P<0.05). Conclusion VEGF can be main-tained in high level after rehabilitation.
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Objective To investigate the stromal cell derived factor 1 α (SDF-1 α) and chemokine CXC motif receptor 4 (CXCR4) axis using acupoint electroacupuncture (EA) on the brains of rats after focal cerebral ischemia and reperfusion.Methods Ninety-eight Sprague-Dawley (SD) rats were randomly divided into a control group (8 rats),a model group (50 rats),and an EA group (40 rats).The animal model of focal brain ischemia-reperfusion was made with all the rats in the model group and EA group by using the filament occlusion technique.The model and EA groups were subdivided into 5 subgroups according to the sampling time points on the 1 st,3rd,7th,14th or 21st day after ischemia-reperfusion.The EA was administered bilaterally to the rat analog of the Hegu point (LI 4) in the EA group.The model and control groups received no special treatment.Immunohistochemical methods were employed to detect CXCR4-positive cells in the model and EA groups.The expressions of SDF-1α and CXCR4 mRNA were detected with RT-PCR methods in the 3rd,7th and 14th day subgroups.Results With the prolongation of reperfusion,SDF-1α mRNA expression in the model group had a single peak-like increase in the ischemic area of the cerebral cortex.It had increased significantly by the 3rd day,reached its peak value at the 7th day and then decreased gradually.SDF-1α mRNA expression in the EA group behaved similarly,but SDF-1 mRNA expression was significantly higher in the EA group than in the other two.In the model and EA groups CXCR4 mRNA relative values were higher at the 7th and 14th day than at day 3,and the expression at day 14 was significantly greater than at day 7.CXCR4 mRNA values in the EA group were significantly higher than in the model group at each time point.The expression of CXCR4-positive cells began to increase on the 1 st day in the model group,reached its peak value at the 7th day,then decreased by day 14,but it was still strongly expressed highly at the 21st day.Compared with the model group,the expression in the EA group showed the same pattern,but the number of CXCR4-positive cells in EA group was significantly higher.Conclusion Point EA can activate the SDF-1α and CXCR4 axis to promote angiogenesis after focal cerebral ischemia and reperfusion,at least in rats.
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10.3969/j.issn.2095-4344.2013.23.021
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Objective To investigate the mechanism by which electro-acupuncture (EA) promotes revascularization in the brain after focal cerebral ischemia and reperfusion.Methods The Sprague-Dawley rat model of focal cerebral ischemia was made by filament occlusion. The rats were randomly divided into a control group, a model group, and an EA group. The model and EA groups were each divided into 5 subgroups receiving reperfusion 1, 3,7, 14 or 21 days after ischemia. EA was given at the bilateral Hegn point (LI 4) in the EA group. The expression of stromal cell-derived factor-1α(SDF-1α) mRNA was detected using a RT-PCR in the 3, 7 and 14 day subgroups.The immunohistochemical method was employed to detect the expression of SDF-1α protein. Results Compared with the control group, expression of SDF-1α protein increased significantly in the model and EA groups. Compared with the model group, the expression of SDF-1α mRNA increased significantly in the 3, 7 and 14 day subgroups.SDF-1α protein expression and microvessel count increased slightly but not significantly in the 1d subgroup, but the increases were significant in the 3, 7, 14 and 21 day subgroups.Conclusions EA may promote angiogenesis in an ischemic area of the cortex by increasing the expression of SDF-1αmRNA and its protein after focal cerebral ischemia and reperfusion.