ABSTRACT
Objective:To evaluate effect of addition and subtraction therapy of Buyang Huanwutang combined with Si Junzitang and acupuncture to poststroke fatigue （PSF） and syndrome of Qi deficiency and blood stasis， at the same time we studied the antioxidant and anti-inflammatory effects. Method:One hundred and forty-four patients were randomly divided into control group and observation group （1∶1） by random number table. 66 patients in control group completed the therapy （4 patients were falling off or missing visit， 2 patients were eliminate）， 67 patients in observation group completed the therapy （2 patients were falling off or missing visit， 3 patients were eliminate）. In control group， patinets got acupuncture， 1 time/day， 6 times/week， they also got Geqi Tongmai grain， 10 g/time， 3 times/day. Patients in observation group got acupuncture （the same as which in control group）， and addition and subtraction therapy of Buyang Huanwutang combined with Si Junzitang， 1 dose/day， and courses of treatment in two groups were 4 weeks. Before and after treatment， fatigue severity scale （FSS）， NIH stroke scale （NIHSS）， syndrome of Qi deficiency and blood stasis， stroke specific quality of life scale （SS-QOL）， and scores of ability of daily life （ADL） were recorded. And levels of superoxide dismutase （SOD）， malondialdehyde （MDA）， glutathione peroxidase （GSH-Px）， homocysteine （Hcy）， interleukin-1β （IL-1β）， IL-6， tumor necrosis factor-α （TNF-α） and C-reactive protein （CRP） were detected. And the safety evaluated. Result:Disease effect in observation group was better than which in control group （Z=2.118， P<0.05）. And effect after using traditional Chinese medicine （TCM） was also better than that in control group （Z=2.046， P<0.05）. Scores of FSS， syndrome of Qi deficiency and blood stasis， NIHSS， and levels of IL-1β， IL-6， Hcy， CRP， TNF-α and MDA in observation group were all lower than those in control group （P<0.01）， and scores of SS-QOL， ADL， and levels of GSH-Px and SOD were all higher than those in control group （P<0.01）. Then there was no related safety issues caused by drug. Conclusion:Addition and subtraction therapy of Buyang Huanwutang combined with Si Junzitang and acupuncture had effect of anti-oxidation and anti-inflammatory， and can significantly reduce fatigue and degree of neurological impairment and can improve patients' quality of life and daily life ability. The clinical effect is significant and safe， which is worthy of further research and application.
ABSTRACT
The effects of endothelin-1 (ET-1) and other drugs on the reactive oxygen species (ROS) generation and cardiomyocyte hypertrophy were examined in experiments on the cultured neonatal rat cardiomyocytes. The role of ROS on neonatal rat cardiomyocyte hypertrophy induced by ET-1 was studied and the relationship of PKC activation and ROS generation was investigated. The level of intracellular ROS was measured by the ROS-specific probe 2',7'-dichlorofluorescin diacetate (DCF-DA). Cardiomyocyte hypertrophy was determined by the RNA content, the total protein of cells and the cell surface area. The results are as follows. The fluorescence intensity of intracellular DCF-DA increased by 77% in cultured neonatal rat cardiac myocytes treated with ET-1 (10 nmol/L) vs control group. Compared with control group, the fluorescence intensity of intracellular PI, protein content and cell surface area increased by 128%, 87% and 151% respectively (all P<0.01) in cardiac myocytes treated with ET-1 (10 nmol/L). ABT-627, CC, or CAT inhibited the ET-1-induced increase in fluorescence intensity of intracellular DCF-DA by 62%,60% and 51% respectively (all P<0.01), and also attenuated the cardiac hypertrophy. The fluorescence intensity of intracellular DCF-DA increased by 74% (P<0.01) in myocytes treated with PMA (1 micromol/L) vs control group. Therefore, in the course of cardiomyocyte hypertrophy, ET-1 increases intracellular ROS in the cultured neonatal rat cardiac myocytes and inhibits cardiomyocyte hypertrophy induced by ROS. The ET(A) and PKC activation mediate the ROS production and cardiomyocyte hypertrophy induced by ET-1. ROS is necessary in the ET-1-induced cardiomyocyte hypertrophy.