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Objective:To observe the clinical effect of Qiangshen Tongdu acupuncture combined with Baixiao moxibustion on lumbar disc herniation.Methods:A total of 72 patients with lumbar disc herniation in the department were enrolled between January 2018 and March 2021. According to random number table method, they were divided into the observation group and control group, 36 in each group. The control group was treated with the routine treatment, while the observation group was treated with Qiangshen Tongdu acupuncture combined with Baixiao moxibustion. The changes in scores of TCM symptoms, pain remission, Japanese Orthopedic Association (JOA), Oswestry disability index (ODI) and quality of life before and after treatment in both groups were observed and recorded.Results:After treatment, scores of all TCM symptoms in the observation group were significantly lower than those in the control group ( t values were 7.29, 2.75, 6.70, 3.33, P<0.01 or P<0.05), score of visual analogue scale was significantly lower than that in the control group ( t values were 2.11, 6.26, P<0.05 or P<0.01), scores of JOA and quality of life were significantly higher than those in the control group ( t=4.39, P<0.01), and ODI score was significantly lower than that in the control group ( t values were 4.74, 4.59, 5.93, 5.42, 4.68, 4.04, 4.73, 5.68, P<0.01). Conclusion:The application of Qiangshen Tongdu acupuncture combined with Baixiao moxibustion can relieve pain, improve clinical symptoms, lumbar function and quality of life in patients with lumbar disc herniation.
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OBJECTIVE To explore the effects of acteoside on hypoxia/reoxygena tion（H/R）-induced cardiomyocyte damage by regulating Rho family GTPase 3（Rnd3）/nuclear factor κB（NF-κB）pathway. METHODS The H 9c2 cardiomyocyte were divided into control group （no administration ，no modeling ），H/R group （only modeling ），H/R+AS-L group ，H/R+AS-M group ， H/R+AS-H group （10，30，90 μmol/L acteoside for above 3 groups firstly ，and then modeling ），H/R+pcDNA group [transfecting pcDNA （empty vector ） firstly，and then modeling] ，H/R + pcDNA-Rnd 3 group [overexpression of Rnd 3 by transfecting pcDNA-Rnd3（Rnd3 overexpression vector ）firstly，and then modeling] ，H/R+AS-H+si-NC group [transfecting si-NC （negative control）firstly，and then giving 90 μmol/L acteoside and modeling]，H/R+AS-H+si-Rnd3 group [inhibiting overexpression of Rnd 3 by transfecting si-Rnd 3 （Rnd3 small interfering RNA ） firstly，and then giving 90 μ mol/L acteoside and modeling]. After corresponding treatment ，the apoptotic rate ，release of lactate dehydrogenase （LDH），malondialdehyde（MDA）level，the activity of superoxide dismutase （SOD），the level of tumor necrosis factor α（TNF-α），interleukin 1β（IL-1β）and interleukin- 6（IL-6）， mRNA and protein expression of Rnd 3 and NF-κB subunit p65（NF-κB p65），the expression of aspartate proteolytic enzyme 3 （Cleaved Caspase- 3）protein and Cleaved Caspase- 9 protein were detected. RESULTS Different concentrations of acteoside could reduce the apoptotic rate of H/R-induced H 9c2 cardiomyocyte，the protein expressions of Cleaved Caspase- 3 and Cleaved Caspase-9，mRNA and protein expressions of NF-κB p65，the levels of LDH release and MDA ，TNF-α，IL-1β and IL-6，while increase the activity of SOD and mRNA and protein expressions of Rnd 3（P＜0.05），in a dose-dependent manner. Overexpression of Rnd 3 could decrease the apoptotic rate of H 9c2 cardiomyocyte，protein expressions of NF-κB p65，Cleaved Caspase- 3 and Cleaved Caspase- 9， the levels of LDH release ， MDA， TNF-α，IL-1β and IL-6，while increase the protein expression of Rnd 3 and the activity of SOD （P＜0.05）. The inhibition overexpression of Rnd 3 could weaken the inhibitory effects of acteoside on H/R-induced apoptosis of H 9c2 cardiomyocyte， oxidative stress and inflammatory reaction （P＜0.05）. CONCLUSIONS Acteoside could regulate Rnd 3/NF-κ B pathway by promoting the expression of Rnd 3 and inhibiting the expression of NF-κB p65，inhibit cardiomyocyte apoptosis ，oxidative stress and inflammation reaction so as to relieve the H/R-induced cardiomyocyte damage.
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Purpose To evaluate the clinical guiding value of 99Tcm-methoxyisobutylisonitrile gated myocardial perfusion imaging (99Tcm-MIBI G-MPI) in diagnosing the coronary microangiopathy in patients with diabetic mellitus.Materials and Methods Sixty patients with clinical confirmed coronary microvascular angina were selected and assigned into two groups,with 26 patients (with diabetes mellitus) in group A and 34 patients in group B (without diabetes mellitus).The region,extent and range of coronary microangiopathy was detected by 99Tcm-MIBI G-MPI,and the difference of myocardial ischemia between the two groups was statistically analyzed.Results The ratio of abnormal myocardial perfusion in group A was significantly higher than that in group B (96.15％ vs.73.53％,x2=5.43,P＜0.05);the total number of abnormal coronary branches in group A was significantly larger than that in group B (82.67％ vs.62.67％,P＜0.05);the total number abnormal perfusion segments in group A was significantly larger than that in group B (P＜0.05),and the abnormal perfusion segments number of anterior wall,septum,apical region and inferior wall in group A was significantly larger than that ingroup B (P＜0.05);the rate of abnormal perfusion at single coronary supplying region in group A was significantly lower than that in group B (P＜0.05).Conclusion 99Tcm-MIBI G-MPI is of great clinical significance for diagnosing coronary microangiopathy and evaluating myocardial ischemia in patients with diabetes mellitus.
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Objective:To explore effect of high glucose on expression of osteoprotegerin (OPG) and receptor activator of NF-毷B ligand (RANKL) in rat aortic vascular smooth muscle cells. Methods: SD rats were intraperitoneally injected with streptozotocin, OPG and RANKL expression in rat thoracic aortas were detected by immunohistochemical staining. In cultured vascular smooth muscle cells (VSMCs) (A7r5), qRT-PCR and Western blot analysis were used to examine the mRNA and protein levels of OPG and RANKL.Results: Our results demonstrated that OPG expression was increased in hyperglycemic rat aortic VSMCs, while RANKL expression was decreased. Besides,in vitroexperiments high glucose induced OPG expression, but depressed RANKL expression by dose- and time-dependent manner in cultured A7r5.Conclusions: Our findings suggested that high glucose could promote the expression of OPG, and inhibit the expression of RANKL in VSMCs, which may be partly be the molecular mechanism of diabetic vascular calcification.