ABSTRACT
Objective:To observe the effect of acupuncture on constipation in children with autism spectrum disorder (ASD). Methods:From January, 2019 to November, 2020, 50 ASD children with constipation from Rehabilitation Center of the Second Affiliated Hospital of Heilongjiang University of Chinese Medicine were admitted and randomly divided into acupuncture-rehabilitation group (n = 25) and medicine-rehabilitation group (n = 25). For constipation, the acupuncture-rehabilitation group used scalp acupuncture, body acupuncture combined with rehabilitation; the medicine-rehabilitation group took probiotics orally combined with rehabilitation. Both groups received conventional rehabilitation for constipation and the core symptoms. Constipation was treated for eight weeks, and ASD symptoms was treated for twelve weeks. After eight weeks and twelve weeks, the efficacy of constipation and the scores of main symptoms of constipation were compared, and they were also evaluated with Autism Child Behavior Scale (ABC) and Autism Treatment Evaluation Scale (ATEC). Results:Before treatment, there was no significant difference in the main symptoms of constipation, nor the scores of ABC and ATEC between two groups (P > 0.05). Eight weeks after treatment, the main symptoms of constipation significantly improved (t > 5.473, P < 0.001); twelve weeks after treatment, the efficacy of constipation and the main symptoms of constipation were better in the acupuncture-rehabilitation group than in the medicine-rehabilitation group (Z = 2.848, t = -2.139, P < 0.05). Eight weeks after treatment, the scores of ABC and ATEC significantly decreased (t > 7.139, P < 0.001), and there was no significant difference between two groups (P > 0.05); the score of behavior of ATEC significantly decreased in the acupuncture-rehabilitation group (t = 3.849, P < 0.01), and was lower than that of the medicine-rehabilitation group (t = -2.643, P < 0.05), and no significant difference in other items was found between two groups (P > 0.05); twelve weeks after treatment, the scores of ABC and ATEC were lower in the acupuncture-rehabilitation group than in the medicine-rehabilitation group (|t| > 2.156, P < 0.05). Conclusion:Acupuncture-rehabilitation can improve the longer-lasting effect of constipation, and also improve the core symptoms of ASD, which is superior to medicine-rehabilitation.
ABSTRACT
Icaritin, a prenylflavonoid derivative from Epimedium Genus, has been shown to exhibit many pharmacological and biological activities. However, the function and the underlying mechanisms of icaritin in human non-small cell lung cancer have not been fully elucidated. The purpose of this study was to investigate the anticancer effects of icaritin on A549 cells and explore the underlying molecular mechanism. The cell viability after icaritin treatment was tested by MTT assay. The cell cycle distribution, apoptosis and reactive oxygen species (ROS) levels were analyzed by flow cytometry. The mRNA and protein expression levels of the genes involved in proliferation and apoptosis were respectively detected by RT-PCR and Western blotting. The results demonstrated that icaritin induced cell cycle arrest at S phase, and down-regulated the expression levels of S regulatory proteins such as Cyclin A and CDK2. Icaritin also induced cell apoptosis characterized by positive Hoechst 33258 staining, accumulation of the Annexin V-positive cells, increased ROS level and alteration in Bcl-2 family proteins expression. Moreover, icaritin induced sustained phosphorylation of ERK and p38 MAPK. These findings suggested that icaritin might be a new potent inhibitor by inducing S phase arrest and apoptosis in human lung carcinoma A549 cells.
ABSTRACT
Fucoidan is one of the main bioactive components of polysaccharides. The current study was focused on the anti-tumor effects of fucoidan on human heptoma cell line HepG2 and the possible mechanisms. Fucoidan treatment resulted in cell cycle arrest and apoptosis of HepG2 cells in a dose-dependent manner detected by MTT assay, flow cytometry and fluorescent microscopy. The results of flow cytometric analysis revealed that fucoidan induced G2/M arrest in the cell cycle progression. Hoechst 33258 and Annexin V/PI staining results showed that the apoptotic cell number was increased, which was associated with a dose-dependent up-regulation of Bax and down-regulation of Bcl-2 and p-Stat3. In parallel, the up-regulation of p53 and the increase in reactive oxygen species were also observed, which may play important roles in the inhibition of HepG2 growth by fucoidan. In the meantime, Cyclin B1 and CDK1 were down-regulated by fucoidan treatment. Down-regulation of p-Stat3 by fucoidan resulted in apoptosis and an increase in ROS in response to fucoidan exposure. We therefore concluded that fucoidan induces apoptosis through the down-regulation of p-Stat3. These results suggest that fucoidan may be used as a novel anti-cancer agent for hepatocarcinoma.
ABSTRACT
Fucoidan is one of the main bioactive components of polysaccharides. The current study was focused on the anti-tumor effects of fucoidan on human heptoma cell line HepG2 and the possible mechanisms. Fucoidan treatment resulted in cell cycle arrest and apoptosis of HepG2 cells in a dose-dependent manner detected by MTT assay, flow cytometry and fluorescent microscopy. The results of flow cytometric analysis revealed that fucoidan induced G2/M arrest in the cell cycle progression. Hoechst 33258 and Annexin V/PI staining results showed that the apoptotic cell number was increased, which was associated with a dose-dependent up-regulation of Bax and down-regulation of Bcl-2 and p-Stat3. In parallel, the up-regulation of p53 and the increase in reactive oxygen species were also observed, which may play important roles in the inhibition of HepG2 growth by fucoidan. In the meantime, Cyclin B1 and CDK1 were down-regulated by fucoidan treatment. Down-regulation of p-Stat3 by fucoidan resulted in apoptosis and an increase in ROS in response to fucoidan exposure. We therefore concluded that fucoidan induces apoptosis through the down-regulation of p-Stat3. These results suggest that fucoidan may be used as a novel anti-cancer agent for hepatocarcinoma.
Subject(s)
Humans , Antineoplastic Agents , Pharmacology , Apoptosis , Blotting, Western , CDC2 Protein Kinase , Genetics , Metabolism , Cyclin B1 , Genetics , Metabolism , Dose-Response Relationship, Drug , Down-Regulation , Flow Cytometry , G2 Phase Cell Cycle Checkpoints , Genetics , Gene Expression Regulation, Neoplastic , Hep G2 Cells , Hepatoblastoma , Genetics , Metabolism , Pathology , Liver Neoplasms , Genetics , Metabolism , Pathology , Microscopy, Fluorescence , Polysaccharides , Pharmacology , Proto-Oncogene Proteins c-bcl-2 , Genetics , Metabolism , Reactive Oxygen Species , Metabolism , Reverse Transcriptase Polymerase Chain Reaction , STAT3 Transcription Factor , Genetics , Metabolism , Tumor Suppressor Protein p53 , Genetics , Metabolism , bcl-2-Associated X Protein , Genetics , MetabolismABSTRACT
Icaritin, a prenylflavonoid derivative from Epimedium Genus, has been shown to exhibit many pharmacological and biological activities. However, the function and the underlying mechanisms of icaritin in human non-small cell lung cancer have not been fully elucidated. The purpose of this study was to investigate the anticancer effects of icaritin on A549 cells and explore the underlying molecular mechanism. The cell viability after icaritin treatment was tested by MTT assay. The cell cycle distribution, apoptosis and reactive oxygen species (ROS) levels were analyzed by flow cytometry. The mRNA and protein expression levels of the genes involved in proliferation and apoptosis were respectively detected by RT-PCR and Western blotting. The results demonstrated that icaritin induced cell cycle arrest at S phase, and down-regulated the expression levels of S regulatory proteins such as Cyclin A and CDK2. Icaritin also induced cell apoptosis characterized by positive Hoechst 33258 staining, accumulation of the Annexin V-positive cells, increased ROS level and alteration in Bcl-2 family proteins expression. Moreover, icaritin induced sustained phosphorylation of ERK and p38 MAPK. These findings suggested that icaritin might be a new potent inhibitor by inducing S phase arrest and apoptosis in human lung carcinoma A549 cells.
Subject(s)
Humans , Antineoplastic Agents, Phytogenic , Pharmacology , Apoptosis , Cell Line, Tumor , Flavonoids , Pharmacology , Lung Neoplasms , Drug Therapy , Metabolism , Pathology , MAP Kinase Signaling System , Neoplasm Proteins , Reactive Oxygen Species , Metabolism , S Phase Cell Cycle CheckpointsABSTRACT
Fucoidan is an active component of seaweed, which inhibits proliferation and induces apoptosis of several tumor cells while the detailed mechanisms underlying this process are still not clear. In this study, the effect of Fucoidan on the proliferation and apoptosis of human breast cancer MCF-7 cells and the molecular mechanism of Fucoidan action were investigated. Viable cell number of MCF-7 cells was decreased by Fucoidan treatment in a dose-dependent manner as measured by MTT assay. Fucoidan treatment resulted in G1 phase arrest of MCF-7 cells as revealed by flow cytometry, which was associated with the decrease in the gene expression of cyclin D1 and CDK-4. Annexin V/PI staining results showed that the number of apoptotic cells was associated with regulation of cytochrome C, caspase-8, Bax and Bcl-2 at transcriptional and translational levels. Both morphologic observation and Hoechst 33258 assay results confirmed the pro-apoptotic effect of Fucoidan. Meanwhile, the ROS production was also increased by Fucoidan treatment, which suggested that Fucoidan induced oxidative damage in MCF-7 cells. The results of present study demonstrated that Fucoidan could induce G1 phase arrest and apoptosis in MCF-7 cells through regulating the cell cycle and apoptosis-related genes or proteins expression, and ROS generation is also involved in these processes.
ABSTRACT
Fucoidan is an active component of seaweed, which inhibits proliferation and induces apoptosis of several tumor cells while the detailed mechanisms underlying this process are still not clear. In this study, the effect of Fucoidan on the proliferation and apoptosis of human breast cancer MCF-7 cells and the molecular mechanism of Fucoidan action were investigated. Viable cell number of MCF-7 cells was decreased by Fucoidan treatment in a dose-dependent manner as measured by MTT assay. Fucoidan treatment resulted in G1 phase arrest of MCF-7 cells as revealed by flow cytometry, which was associated with the decrease in the gene expression of cyclin D1 and CDK-4. Annexin V/PI staining results showed that the number of apoptotic cells was associated with regulation of cytochrome C, caspase-8, Bax and Bcl-2 at transcriptional and translational levels. Both morphologic observation and Hoechst 33258 assay results confirmed the pro-apoptotic effect of Fucoidan. Meanwhile, the ROS production was also increased by Fucoidan treatment, which suggested that Fucoidan induced oxidative damage in MCF-7 cells. The results of present study demonstrated that Fucoidan could induce G1 phase arrest and apoptosis in MCF-7 cells through regulating the cell cycle and apoptosis-related genes or proteins expression, and ROS generation is also involved in these processes.