ABSTRACT
The purpose of the study is to analyze the outcomes of randomized controlled trial(RCT) of Chinese herbal medicine formula(CHMF) in the treatment of vascular cognitive impairment caused by cerebral small vessel disease(CSVD-VCI), and provide suggestions for future studies in this field. Three English databases, four Chinese databases, and two online registration websites of clinical trials were searched with use of the search strategy established in advance. Relevant RCTs published in recent ten years were screened, and necessary information was extracted to assess the risk of bias and analyze the outcomes of these RCTs. As a result, a total of 10 461 articles were retrieved, of which 8 681 were kept after de-duplication, and 41 RCTs were included after screening, with a generally higher risk of bias. The outcomes of included RCTs were classified into 9 categories, namely, clinical symptom outcomes, neuroimaging outcomes, neuroelectrophysiological outcomes, blood biochemical outcomes, hemorheology outcomes, physical signs, syndrome scores of traditional Chinese medicine(TCM), clinical effective rate, and safety outcomes. Among them, the most frequently reported outcomes of included RCTs were blood biochemical outcomes, and clinical symptom outcomes showed the highest reporting rate. Besides, 9 RCTs reported syndrome scores of TCM as the outcomes and illustrated corresponding evaluation criteria. The analysis showed that the application of RCT outcomes in this field had clinical rationality and limitations, and there were also some deficiencies in the trial design level, namely, no distinction between primary and secondary outcomes, insufficient blind methods, not detailed description of outcomes, disunity of evaluation tools, and despised endpoint outcomes. These limitations and deficiencies were negatively affecting the quality of RCTs of CHMF in the treatment of CSVD-VCI. Therefore, we suggest that future researchers should be well prepared in the top-level design stage, and actively construct the core outcome set of this field, so as to improve the quality of clinical trials.
Subject(s)
Humans , Cerebral Small Vessel Diseases , Cognitive Dysfunction , Drugs, Chinese Herbal , Medicine, Chinese Traditional , PhytotherapyABSTRACT
Wumei Pills is a prescription for the treatment of ascariasis of biliary tract and chronic diarrhea. It can be widely used in the treatment of many diseases with the basic pathogenesis "simultaneous occurrence of cold and heat" because of its features of cold-heat combination and tonifying-purgation combination. What should be noticed is that it is necessary to use large dose of Mume Fructus, which is also can be applied to the treatment of chronic diseases. Carefully sticking to pathogenesis in clinical treatment can obtain good efficacy.
ABSTRACT
Objective To evaluate the effects of electroacupuncture on clinical efficacy, changes of serum vascular endothelial growth factor (VEGF) and neuron specific enolase (NSE) in patients with acute cerebral infarction. Methods From January 2015 to June 2016, 96 patients with acute cerebral infarction were selected and randomly divided into control group (48 cases) and electroacupuncture group (48 cases). The control group was given routine treatment, and the electroacupuncture group was given acupuncture combined with scalp acupuncture and body acupuncture on the basis of routine treatment for two weeks. The clinical efficacy, NIHSS score, serum VEGF and NSE levels were evaluated in two groups of patients. Results After two weeks of treatment, the clinical effective rate was higher in electroacupuncture group than that of the control group (P<0.05). After one week and two weeks of treatment, the NIHSS score and serum NSE level were significantly decreased in both groups of patients compared with those before treatment (P<0.05). The NIHSS score and serum NSE level were lower in the electroacupuncture group than those in the control group (P<0.05). After one week and two weeks of treatment, serum VEGF levels were significantly increased compared with those before treatment in the two groups (P<0.05). The serum VEGF level was higher in electroacupuncture group than that in control group (P<0.05). Conclusion Electroacupuncture treatment can promote the regeneration of damaged blood vessels, repair neurons and improve clinical efficacy in patients with acute cerebral infarction, which shows definite clinical significance.
ABSTRACT
Aim To study the inhibitory effect of volatile components in Oroxyli Semen on liver cancer and its possible mechanisms.Methods H22 bearing mouse model was used,the mice were divided into six groups:blank,model,positive (cytoxan,100 mg · kg-1),low-,mid-,and high-dose (17.5,35,and 70 mg · kg-1) volatile components groups,and then the mice were ig given once daily for consecutive 12 d.Then the tumor growth inhibitory rate,spleen and thymus indexes were calculated;the serum levels of IL-2,IL-6 were determined.HE staining was used to study of the apoptosis of the solid tumor.After treatment of SMMC-7721 cells with 0 ～ 1 g · L-1 of volatile components for 24,48 and 72 h,MTT assay was used to examine the proliferation.TUNEL method was applied to detect cell apoptosis,and RT-PCR method to detect Bax,Bcl-2,caspase-3 mRNA experssion.Results The inhibitory rate of volatile components high-dose on H22 bearing mice was 42.08％.The thymus index and the contents of serum IL-2 and IL-6 of H22 bearing mice were significantly higher than those in model group.Volatile components could significantly inhibit proliferation and induce apoptosis of SMMC-7721 cells,downregulate the expression of Bcl-2 mRNA,and up-regulate the expression of Bax,caspase-3 mRNA.Conclusions The volatile components in Oroxyli Semen have obvious anti-tumor activity in vitro and in vivo,and its mechanism may be related to enhancing immune system and promoting tumor cell apoptosis.
ABSTRACT
AIM:To explore the role of ubiquitin E3 ligase tripartite motif 10 (TRIM10) in the development of cardiomyocyte hypertrophy .METHODS: Primary cultured neonatal rat cardiomyocytes ( NRCMs ) were infected with siRNA-TRIM10, siRNA-control, Ad-TRIM10 or Ad-GFP for 24 h respectively, and then stimulated with phenylephrine ( PE) for additional 24 h.The protein levels of TRIM10, AKT and ERK1/2 were determined by Western blot .The size of the NRCMs was measured by immunofluorescence staining .The mRNA expression of atrial natriuretic peptide ( ANP) and brain natriuretic peptide ( BNP) was detected by RT-qPCR.RESULTS:Compared with the control , PE treatment signifi-cantly increased the protein expression of TRIM 10.Moreover, transfection of NRCMs with siRNA-TRIM10 markedly inhibi-ted cardiomyocyte size , the mRNA expression of ANP and BNP , and the phosphorylation levels of AKT and ERK as com-pared with siRNA-control after PE treatment.In contrast, overexpression of TRIM10 significantly enhanced PE-induced hy-pertrophic effect on NRCMs above .CONCLUSION:TRIM10 regulates cardiomyocyte hypertrophy partially through AKT and ERK signaling pathways .
ABSTRACT
AIM:To explore the role of ubiquitin E3 ligase tripartite motif 10 (TRIM10) in the development of cardiomyocyte hypertrophy .METHODS: Primary cultured neonatal rat cardiomyocytes ( NRCMs ) were infected with siRNA-TRIM10, siRNA-control, Ad-TRIM10 or Ad-GFP for 24 h respectively, and then stimulated with phenylephrine ( PE) for additional 24 h.The protein levels of TRIM10, AKT and ERK1/2 were determined by Western blot .The size of the NRCMs was measured by immunofluorescence staining .The mRNA expression of atrial natriuretic peptide ( ANP) and brain natriuretic peptide ( BNP) was detected by RT-qPCR.RESULTS:Compared with the control , PE treatment signifi-cantly increased the protein expression of TRIM 10.Moreover, transfection of NRCMs with siRNA-TRIM10 markedly inhibi-ted cardiomyocyte size , the mRNA expression of ANP and BNP , and the phosphorylation levels of AKT and ERK as com-pared with siRNA-control after PE treatment.In contrast, overexpression of TRIM10 significantly enhanced PE-induced hy-pertrophic effect on NRCMs above .CONCLUSION:TRIM10 regulates cardiomyocyte hypertrophy partially through AKT and ERK signaling pathways .
ABSTRACT
<p><b>OBJECTIVE</b>This study was to explore the effect of arsenic trioxide (ATO; As(2)O(3)) on differentiation of chronic myeloid leukemia K562 cells and its potential mechanism.</p><p><b>METHODS</b>ATO with different concentration (0.1, 0.5, 1.0, 2.0, 5.0 µmol/L) were used to treat K562 cells, and MTT assay was used to detect the growth level of K562 cells; Benzidine staining was applied to measure the change of hemoglobin content; flow cytometry (FCM) was conducted to detect the expression of CD41 and GPA on K562 cells; RT-PCR and Western blot were used to measure the mRNA expression of BTG1 and TAL1 and the protein expression of BTG1 and TAL1, respectively.</p><p><b>RESULTS</b>ATO significantly inhibited the growth of K562 with dose- and time- dependent manners by benzidine staining, the positive rate of K562 cells induced by ATO reached to 17.63% ± 1.18%, which was significantly higher than that of control (2.87% ± 0.63%) (P < 0.01), and GPA, as the specific marker of erythroid cell differentiation, achieved 68.46% ± 3.67%, while it in control was 3.39% ± 0.84% (P < 0.01), besides, the CD41 expression of megakaryocyte increased but not so obvious as GPA. Meanwhile, the differentiation-related transcriptional factors TAL1 and BTG1 mRNA and the corresponding proteins were expressed more highly.</p><p><b>CONCLUSION</b>ATO can induce the differentiation of K562 cells into erythroid cells and megakaryocyte, which is associated with up-regulation of the related transcription factors TAL1 and BTG1.</p>
Subject(s)
Humans , Arsenicals , Cell Differentiation , K562 Cells , Leukemia, Myelogenous, Chronic, BCR-ABL Positive , Megakaryocytes , Oxides , RNA, Messenger , Transcription Factors , Up-RegulationABSTRACT
This study was purposed to explore the effect of specific small interfering RNA targeting at bcr-abl fusion gene and its combination with p27 gene clone on the proliferation, cell cycle and apoptosis of chronic myeloid leukemia (CML) cell line K562. CML cell line K562 was used as the study object. A 21nt siRNA targeting at the fusion site of b3:a2 mRNA in bcr-abl fusion gene was designed, synthesized and transfected into the K562 cells as RNA interference group. Northern blot was used to detect the bcr-abl fusion gene, Western blot was used to detect the expression of P210 protein and apoptosis-related protein BCL-xL after the transfection. Meanwhile, p27 gene was amplified from peripheral blood mononuclear cells by RT-PCR, and was confirmed to be correct by sequencing, then p27-pcDNA3.1 vector was constructed and transfected into K562 cell line by Lipofectin. After being selected with G418, p27-pcDNA3.1-K562 cell clone stably expressing p27 was isolated. P27 protein was identified by Western blot. Finally, siRNA and p27 gene clone were together applied to K562 cells, the cell survival rate was tested by MTT. The cell cycle and the apoptosis were tested by flow cytometry. The result showed that in contrast with the control group, the expression level of bcr-abl fusion gene was much lower in siRNA group, about 18.4% of K562 cells in siRNA group were apoptotic at 24 hours after siRNA transfection, and the expression of apoptosis-associated protein BCL-xL was greatly down-regulated. The expression of P27 protein could be detected by Western blot in p27-pcDNA3.1-K562 cells. The strong inhibition of cell proliferation was observed in p27-pcDNA3.1-K562 cells, as compared with control K562 cells. The count of p27-pcDNA3.1-K562 cells in G(0)/G(1) phase increased apparently, but that in S phase declined greatly. Cell cycle was arrested in G(0)/G(1) phase. After the combination of p27-pcDNA3.1-K562 cells with specific siRNA, the percentage of apoptosis obviously increased and cell survival rate significantly declined. It is concluded that the specific siRNA distinctly inhibits the expression of bcr-abl fusion gene, and can induce K562 cell apoptosis. The combination of specific siRNA with P27 gene clone displays a synergy of inhibition and pro-apoptosis effects to K562 cells.