期刊：
Journal of Molecular Neuroscience,2021年71(10):2172-2172 ISSN：0895-8696
通讯作者：
Peng Zhang
作者机构：
[Zhang, Peng; Ye, Haimin; Kang, Zhen] Hunan Univ Chinese Med, Affiliated Hosp 2, 233 Cai E North Rd, Changsha 410005, Hunan, Peoples R China.;[Chen, Tao] Hunan Univ Tradit Chinese Med, Changsha 410208, Peoples R China.
通讯机构：
[Peng Zhang] T;The Second Affiliated Hospital of Hunan University of Chinese Medicine, Changsha, China
期刊：
Journal of Molecular Neuroscience,2021年71(10):2165-2171 ISSN：0895-8696
通讯作者：
Peng Zhang
作者机构：
[Zhang, Peng; Ye, Haimin; Kang, Zhen] Hunan Univ Chinese Med, Affiliated Hosp 2, 233 Cai E North Rd, Changsha 410005, Hunan, Peoples R China.;[Chen, Tao] Hunan Univ Tradit Chinese Med, Changsha 410208, Peoples R China.
通讯机构：
[Zhang, Peng] T;The Second Affiliated Hospital of Hunan University of Chinese Medicine, No. 233 Cai E North Road, Changsha, 410005, Hunan Province, China.
关键词：
Siguan acupoints;Post-stroke depression;Hippocampus;Brain-derived neurotrophic factor;Tyrosine receptor kinase B
摘要：
To study the effect of electroacupuncture at the Siguan acupoints on the expression of hippocampal brain-derived neurotrophic factor (BDNF) and tyrosine receptor kinase B (TrkB) in post-stroke depression (PSD) rats, in order to explore its possible mechanism Fifty specific pathogen-free (SPF)-grade adult male Sprague-Dawley (SD) rats were randomly divided into a blank group, stroke group, PSD group, Siguan acupoint group and fluoxetine group according to the random number method. PSD rats were modeled with middle cerebral artery occlusion combined with chronic unpredictable mild stress. After successful modeling, electroacupuncture was applied to Siguan acupoints for a total of 21days at 30min/session/day. The rats in the fluoxetine group were fed intragastrically according to body weight, once a day, for a total of 21days. The rats in each group were bound and intragastrically administered distilled water every day. The depressive behavior of rats was measured according to the horizontal and vertical scores of the open field test and the sucrose water consumption, and the changes in the number of BDNF- and TrkB-positive cells in the hippocampus of rats were observed by immunohistochemistry. After modeling, the behavioral indicators and the numbers of BDNF- and TrkB-positive cells in each model group were significantly lower than those in the blank group (P < 0.01). After treatment, the behavioral indicators and the numbers of BDNF- and TrkB-positive cells in the Siguan acupoint group and fluoxetine group were significantly higher than that in the PSD group (P < 0.01). During the treatment, the horizontal and vertical scores of the Siguan acupoint group were significantly increased on the seventh day of treatment, and the difference was statistically significant when compared with the PSD group (P < 0.05). The sucrose water consumption was significantly increased on the 14th day of treatment, and the difference was significant when compared with the PSD group (P < 0.05), both of which were earlier than that in the fluoxetine group. During the treatment, there was no significant difference between the two groups (P > 0.05). Electroacupuncture at Siguan acupoints has the same antidepressant effect as fluoxetine, and is more effective than fluoxetine in relieving depression in PSD rats. Its mechanism may be related to the activation of the expression of BDNF and its receptor TrkB.
摘要：
OBJECTIVE: Circular RNA (circRNA) has been found to be involved in regulating tumor development. However, the roles and underlying mechanisms of circRNA in colorectal cancer (CRC) development remain unclear. In this study, we investigated the effects of hsa_circ_0031787 on CRC.a METHODS: Aberrant circRNA expression was explored by the Gene Expression Omnibus (GEO) database, and hsa_circ_0031787 was selected for further study. Hsa_circ_0031787 expression was determined in CRC tissues and cell lines by qRT-PCR. Cell proliferation was measured by Edu and colony formation assays. Cell invasion was tested by Transwell assays. RESULTS: Hsa_circ_0031787 expression levels in CRC were significantly increased and correlated with advanced TNM stage and lymph node metastasis in CRC patients. Functional assays showed that hsa_circ_0031787 suppression reduced CRC cell proliferation and invasion in vitro and reduced tumor growth in vivo. Furthermore, hsa_circ_0031787 suppression reduced activation ofthe Wnt/β-catenin axis in CRC. CONCLUSIONS: Our results showed that hsa_circ_0031787 may function as an oncogenic circRNA in CRC progression, thus providing a new potential therapeutic target.
摘要：
Astragaloside (AST) is derived from the Chinese herb <em>Astragalusmembranaceus</em>, and studies have demonstrated that it promotes differentiation of bone marrow‑derived mesenchymal stem cells (BMSCs). To the best of our knowledge, however, the functions of the component AST‑IV in osteogenesis have not previously been elucidated. The present study aimed to verify the effects of AST‑IV in osteogenesis. First, the proliferation and differentiation status of human BMSCs incubated with AST‑IV were analysed and compared with a control (no AST‑IV treatment). In order to determine the involvement of the glycogen synthase kinase(GSK)3β signalling pathway in AST‑IV, overexpression and inhibition of GSK3β was induced during incubation of BMSCs with AST‑IV. In order to investigate how neuronal growth factor (NGF) contributes to BMSCs differentiation, BMSCs were co‑incubated with an anti‑NGF antibody and AST IV, and then levels of osteogenesis markers were assessed. The results demonstrated for the first time that AST‑IV contributed to BMSCs differentiation. Furthermore, the GSK3β/β‑catenin signalling pathway was revealed to be involved in AST‑IV‑induced osteogenesis; moreover, AST‑IV accelerated differentiation by enhancing the expression levels of NGF. In summary, the present study demonstrated that AST‑IV promotes BMSCs differentiation, thus providing a potential target for the treatment of osteoporosis.
作者机构：
[Huang, Pan; Wang, Chang; Zhou, Rong; Yang, Zhibo; Luo, Meijunzi] Hunan Univ Chinese Med, Dept Dermatol, Affiliated Hosp 2, Changsha 410005, Hunan, Peoples R China.;[Chen, Zhenping] Hunan Univ Chinese Med, Clin Tradit Chinese Med Coll 2, Changsha 410005, Hunan, Peoples R China.
通讯机构：
[Chang Wang] D;Department of Dermatology, The Second Affiliated Hospital of Hunan University of Chinese Medicine, Changsha, Hunan Province 410005, China
摘要：
Psoriasis is a chronic immune-mediated inflammatory dermatosis. STAT3 has been considered a critical regulator of psoriasis pathogenesis due to its role in inflammation and immune responses. Furthermore, alongside noncoding RNAs, including long non-coding RNAs (lncRNAs) and miRNAs, STAT3 also plays a critical role in psoriasis pathogenesis. Two sets of online microarray profiles (GSE50790 and GSE13355) were subsequently downloaded and analyzed to search for lncRNAs upregulated in psoriasis lesion tissues. The expression of lncRNA SH3PXD2A-AS1 could be remarkably upregulated in psoriasis specimens. SH3PXD2A-AS1 silence was found to suppress HaCaT cell proliferation and promote HaCaT cell apoptosis significantly. Meanwhile, SH3PXD2A-AS1 silence significantly increased cleaved-caspase-3 protein levels and inhibited S100A7, TNF-alpha, IL-6, p-STAT3, STAT3, CyclinD1, and survivin protein levels. Moreover, the expression of miR-125b could be substantially decreased within psoriasis lesion tissue samples, while miR-125b could negatively regulate the SH3PXD2A-AS1 and STAT3 expression. As predicted by an online tool and validated by luciferase reporter and RIP assays, miR125b was found to bind to SH3PXD2A-AS1 and STAT3 3 ' UTR directly; SH3PXD2A-AS1 competed with 3 ' UTR of STAT3 for miR-125b binding to counteract miR-125b-mediated suppression of STAT3. STAT3 is known to activate the transcription of SH3PXD2A-AS1 through the targeting of its promoter region. It consequentially forms a regulatory feedback loop promoting SH3PXD2A-AS1 expression affecting HaCat cell proliferation and apoptosis. A novel STAT3 related mechanism whereby STAT 3/ SH3PXD2A-AS1/ miR-125b/STAT3 positive feedback loop which could potentially affect the pathogenesis of Psoriasis has been established.
期刊：
Frontiers in Oncology,2021年11:643941 ISSN：2234-943X
通讯作者：
Yi, Xiaoping;Zhu, Liping;Liu, Haipeng
作者机构：
[Zhu, Liping; Chen, Changyong; Zeng, Feiyue; Yi, Xiaoping; Zhu, LP; Liu, HP; Liu, Haipeng] Cent South Univ, Xiangya Hosp, Dept Radiol, Changsha, Peoples R China.;[Zhu, Liping; Yi, Xiaoping; Zhu, LP; Liu, HP; Liu, Haipeng] Cent South Univ, Xiangya Hosp, Natl Clin Res Ctr Geriatr Disorders, Changsha, Peoples R China.;[Yi, Xiaoping] Xiangya Hosp, Hunan Key Lab Skin Canc & Psoriasis, Changsha, Peoples R China.;[Yi, Xiaoping] Xiangya Hosp, Hunan Engn Res Ctr Skin Hlth & Dis, Changsha, Peoples R China.;[Chen, Qiurong] Sun Yat Sen Univ, Zhongshan Ophthalm Ctr, State Key Lab Ophthalmol, Guangzhou, Peoples R China.
通讯机构：
[Yi, XP; Zhu, LP; Liu, HP] C;[Yi, Xiaoping] X;Cent South Univ, Xiangya Hosp, Dept Radiol, Changsha, Peoples R China.;Cent South Univ, Xiangya Hosp, Natl Clin Res Ctr Geriatr Disorders, Changsha, Peoples R China.;Xiangya Hosp, Hunan Key Lab Skin Canc & Psoriasis, Changsha, Peoples R China.
关键词：
Sarcopenia;Body Composition;Platinum-based chemotherapy;progressive disease;non-small-cell lung cancer
摘要：
Background It is prudent to identify the risk for progressive disease (PD) in patients with non-small-cell lung cancer (NSCLC) who undergo platinum-based chemotherapy. The present study aimed to develop a CT imaging-based sarcopenic nomogram for predicting the risk of PD prior to chemotherapy treatment.</p> Methods We retrospectively enrolled patients with NSCLC who underwent platinum-based chemotherapy. Imaging-based body composition parameters such as skeletal muscle index (SMI) for assessment of sarcopenia were obtained from pre-chemotherapy chest CT images at the level of the eleventh thoracic vertebral body (T11). Sarcopenic nomogram was constructed using multivariate logistic regression and performance of the nomogram was evaluated by discrimination, calibration curve, and decision curve.</p> Results Sixty (14.7%) of the 408 patients in the study cohort developed PD during chemotherapy. The prediction nomogram for developing PD achieved a moderate efficiency with an area under the curve (AUC) of 0.75 (95% CI: 0.69-0.80) for the training cohort, and 0.76 (95%CI: 0.68-0.84) for the validation cohort, as well as a good performance of consistence (bootstrap for training cohort: 0.75 +/- 0.02; validation cohort: 0.74 +/- 0.06). Favorable clinical application was observed in the decision curve analysis.</p> Conclusion Our CT-based sarcopenic nomogram showed the potential for an individualized prediction of progression for patients with NSCLC receiving platinum-based chemotherapy.</p>
摘要：
<b><i>Background:</i></b> Osteoarthritis (OA) is the most common joint disorder characterized by degeneration of the articular cartilage and joint destruction with an associated risk of mobility disability in elderly people. Although a lot of achievements have been made, OA is still regarded as an incurable disease. Therefore, the pathological mechanisms and novel therapeutic strategies of OA need more investigation. <b><i>Methods:</i></b> MTT assay was conducted to measure the viability of chondrocytes after LPS treatment. Cell apoptosis was analyzed by annexin V/propidium iodide labeling. ELISA was used to determine the concentrations of interleukin (IL)-1β, IL-6, and tumor necrosis factor (TNF)-α in the culture supernatant of chondrocytes. The expression level of miR-155, IL-1β, FOXO3, TNF-α, IL-6, caspase-3, and caspase-9 in chondrocytes was analyzed by RT-qPCR or Western blot. <b><i>Results:</i></b> We found that LPS led to inflammatory responses, cell apoptosis, and increased miR-155 expression in human articular chondrocytes. Tanshinone IIA could inhibit LPS-induced inflammation and cell apoptosis of chondrocytes via regulating the expression of miR-155 and FOXO3. miR-155 directly targeted the 3′-UTR of FOXO3 to regulate its expression. <b><i>Conclusions:</i></b> Taken together, our data suggest tanshinone IIA ameliorates inflammation response in OA via inhibition of the miR-155/FOXO3 axis, and provide some evidences that tanshinone IIA could be designed and developed as a new promising clinical therapeutic drug for OA patients.
期刊：
Translational Cancer Research,2021年10(1):57-64 ISSN：2218-676X
通讯作者：
Guo, Yihang;Hu, Gui
作者机构：
[Xie, Biao] Hunan Univ Chinese Med, Affiliated Hosp 2, Dept Anorectal Surg 1, Changsha, Peoples R China.;[Hu, Gui; Guo, Yihang; Gong, Ni; Hu, G] Cent South Univ, Xiangya Hosp 3, Dept Gastrointestinal Surg, Tongzipo Rd, Changsha, Peoples R China.
通讯机构：
[Guo, YH; Hu, G] C;Cent South Univ, Xiangya Hosp 3, Dept Gastrointestinal Surg, Tongzipo Rd, Changsha, Peoples R China.
关键词：
Colorectal cancer (CRC);microRNA-133b;mesenchymal-to-epithelial transition;diagnostic biomarker discovery
摘要：
Background: Inactivation of the tumor suppressor gene microRNA-133b is a frequent event in various malignancies including colorectal cancer (CRC). The result of our previous research has found a statistically significant downregulation of microRNA-133b expression in human CRC cells, microRNA-133b can block the growth and metastatic progression of CRC cells in vitro and in vivo by targeting and repressing mesenchymal to epithelial transition factor. In this study, we identify the association between microRNA-133b, epithelial transition Factor expression and clinicopathological parameters. Methods: The detection of microRNA-133b and epithelial transition factor between gene and protein expression was evaluated in 46 patients with CRC. The correlation among microRNA-133b, epithelial transition factor and clinicopathological parameters associated with CRC was assessed. Furthermore, the diagnostic capability of rnicroRNA-133b and epithelial transition factor in CRC was also evaluated. Results: The results show decreased microRNA-133b expression in CRC tissues, and a very strong inverse correlation between the expression of oncogene epithelial transition factor and the expression of microRNA-133b. We also observed that the expression levels of microRNA-133b and epithelial transition factor were statistical associated with clinical stage and lymph node metastasis in CRC tissues, and further identified microRNA-133b and/or epithelial transition factor may be useful for distinguishing CRC patients from the normal population by receiver operating characteristic (ROC) curve analysis. Conclusions: microRNA- 1336 expression is inversely correlated with epithelial transition factor expression. MicroRNA-133b and/or epithelial transition factor may be useful as valuable prognostic biomarkers in CRC patients.
作者机构：
[Li, Bing; Yu, Ya-Nan; Liu, Jun; Wang, Yong-Yan; Dang, Hai-Xia; Wang, Zhong] China Acad Chinese Med Sci, Inst Basic Res Clin Med, Beijing, Peoples R China.;[Li, Dan-Dan; Chen, Yun-Dai; Dong, Wei; Liu, Yu-Qi] Chinese Peoples Liberat Army Gen Hosp, Dept Cardiol, Beijing, Peoples R China.;[Wu, Yang; Tang, Da-Xuan] Beijing Univ Chinese Med, Dongfang Hosp Affiliated, Dept Cardiol, Beijing, Peoples R China.;[Zhang, Fu-Chun; Qiu, Meng] Peking Univ Third Hosp, Dept Geratol, Beijing, Peoples R China.;[He, Jing-Yu; Hua, Qi] Capital Med Univ, Xuan Wu Hosp, Dept Cardiol, Beijing, Peoples R China.
通讯机构：
[Wang, Zhong; Wang, Yong-Yan] I;[Chen, Yun-Dai] D;Institute of Basic Research in Clinical Medicine, China Academy of Chinese Medical Sciences, Beijing, China.;Department of Cardiology, Chinese PLA General Hospital, Beijing, China.
摘要：
It's a challenge for detecting the therapeutic targets of a polypharmacological drug from variations in the responsed networks in the differentiated populations with complex diseases, as stable coronary heart disease. Here, in an adaptive, 31-center, randomized, double-blind trial involving 920 patients with moderate symptomatic stable angina treated by 14-day Danhong injection(DHI), a kind of polypharmacological drug with high quality control, or placebo (0.9% saline), with 76-day following-up, we firstly confirmed that DHI could increase the proportion of patients with clinically significant changes on angina-frequency assessed by Seattle Angina Questionnaire (ΔSAQ-AF ≥ 20) (12.78% at Day 30, 95% confidence interval [CI] 5.86-19.71%, P = 0.0003, 13.82% at Day 60, 95% CI 6.82-20.82%, P = 0.0001 and 8.95% at Day 90, 95% CI 2.06-15.85%, P = 0.01). We also found that there were no significant differences in new-onset major vascular events (P = 0.8502) and serious adverse events (P = 0.9105) between DHI and placebo. After performing the RNA sequencing in 62 selected patients, we developed a systemic modular approach to identify differentially expressed modules (DEMs) of DHI with the Z(summary) value less than 0 compared with the control group, calculated by weighted gene co-expression network analysis (WGCNA), and sketched out the basic framework on a modular map with 25 functional modules targeted by DHI. Furthermore, the effective therapeutic module (ETM), defined as the highest correlation value with the phenotype alteration (ΔSAQ-AF, the change in SAQ-AF at Day 30 from baseline) calculated by WGCNA, was identified in the population with the best effect (ΔSAQ-AF ≥ 40), which is related to anticoagulation and regulation of cholesterol metabolism. We assessed the modular flexibility of this ETM using the global topological D value based on Euclidean distance, which is correlated with phenotype alteration (r(2): 0.8204, P = 0.019) by linear regression. Our study identified the anti-angina therapeutic module in the effective population treated by the multi-target drug. Modular methods facilitate the discovery of network pharmacological mechanisms and the advancement of precision medicine. (ClinicalTrials.gov identifier: NCT01681316).
摘要：
Cutaneous malignant melanoma is a malignancy with one of the fastest increasing incidence rates worldwide; however, the mechanism underlying the occurrence and development of melanoma remains unclear. The aim of the present study was to identify novel biomarkers for the occurrence and development of melanoma. The results of the present study demonstrated that the expression levels of microRNA (miR)-27b were decreased in melanoma tissue samples compared with those in adjacent noncancerous tissue samples and cells according to online and experimental data. By contrast, MYC expression levels were upregulated in melanoma compared with those in adjacent noncancerous tissue samples. miR-27b overexpression significantly inhibited A375 and A2085 melanoma cell DNA synthesis, viability and invasive ability. Dual-luciferase reporter assay results demonstrated that miR-27b inhibited MYC expression through binding to the 3'-untranslated region of MYC mRNA. MYC knockdown in melanoma cells exerted similar effects to those of miR-27b overexpression on DNA synthesis, cell viability and invasive ability; the effects of miR-27b inhibition were significantly reversed by MYC knockdown. In conclusion, the miR-27b/MYC axis may modulate malignant melanoma cell biological behaviors and may be a potential target for melanoma treatment.
摘要：
The prognosis of advanced colorectal cancer (CRC) is currently still very poor, which suggests that the biological mechanisms of CRC oncogenesis are not fully understood. This study was conducted to explore the regulatory effect of SOX-17 on the expression of microRNA (miR)-302b-3p, and the involvement of SOX-17 in the invasion and apoptosis of CRC cells. The expression of SOX-17 and miR-302a,b,c,d-3p in colorectal cancer and normal colon epithelial cell lines was measured by real-time polymerase chain reaction and/or western blot. The regulatory effects of SOX-17 on miR-302b-3p gene in HT29 and LoVo cells were tested using the ChiP assay. The biological activities of SOX-17 and miR-302b-3p were evaluated by invasion and apoptosis assay. Results showed that transfection of SOX-17 small interfering RNA (siSOX-17) significantly increased, whereas transfection of SOX-17 overexpression vector (oeSOX-17) significantly decreased, miR-302b expression in HT29 and LoVo cells. Cotransfection of oeSOX-17 and miR-302b-3p inhibitor (INmiR-302b) significantly blocked the effects of SOX-17 in HT29 and LoVo cells. ChIP experiments showed that SOX-17 bonded to the miR-302b-3p promoter in HT29 and LoVo cells. Transfection of oeSOX-17 and miR-302b-3p mimics (MImiR-302b) significantly decreased, whereas transfection of siSOX-17 and INmiR-302b significantly increased, the invasion of HT29 and LoVo cells. In contrast, transfection of oeSOX-17 and MImiR-302b significantly increased, while transfection of siSOX-17 and INmiR-302b significantly decreased, apoptosis in HT29 and LoVo cells. Cotransfection of oeSOX-17 and INmiR-302b significantly blocked the effects of oeSOX-17 on cell invasion and apoptosis in HT29 and LoVo cells. These results suggested that SOX-17 can bind to the promoter of miR-302b-3p gene to regulate its expression, while both SOX-17 and miR-302b regulate the invasion and apoptosis in colorectal cancer cells.
摘要：
BACKGROUND: During psoriasis initiation and development, deregulations in signaling pathways and gene expression are observed. METHODS: Herein, we downloaded seven sets of microarray mRNA expression profiles showing differentially-expressed genes in psoriasis lesion skin and non-lesion skin tissues and three sets of RNA-seq data and analyzed these online data attempting to screen for crucial genes related to keratinocyte proliferation and psoriasis development. The expression of CTNNBIP1 in psoriasis patients and IMQ mouse model skin tissues were examined by RT-PCR, immunoblotting and IHC. The functions of CTNNBIP1 on HaCaT cell proliferation, apoptosis and β-catenin/TCF-complex were measured by MTT, EdU, flow cytometry, IF, luciferase assays and immunoblotting. RESULTS: The expression of catenin beta interacting protein 1 (CTNNBIP1) was remarkably downregulated within psoriasis lesion skin tissue samples compared to that within non-lesion skin tissues based on both online data and experimental results. In response to a period of different therapies, respectively, CTNNBIP1 expression could be rescued in lesion skin tissues. Within IMQ-induced psoriasis-like dermatitis in mice, CTNNBIP1 silence further aggravated psoriatic phenotypes. In human immortalized keratinocytes, HaCaT cells, CTNNBIP1 silence significantly inhibited cell apoptosis and promoted cell proliferation. Regarding the molecular mechanism, CTNNBIP1 silence in HaCaT cells promoted β-catenin nucleus translocation, enhanced the transcriptional activity of TCF4, and increased β-catenin/TCF-complex downstream c-Myc and cyclin D1 proteins, and also increased the expression of cell proliferation marker ki-67. In contrast to CTNNBIP1, the expression of c-Myc and cyclin D1 showed to be dramatically upregulated within psoriasis lesion tissue samples than that within non-lesion tissue samples. Within tissues, c-Myc and cyclin D1 showed to be negatively correlated with CTNNBIP1, respectively. CONCLUSIONS: We identify CTNNBIP1 as an abnormally downregulated gene in psoriasis. CTNNBIP1 silence significantly disturbs the proliferation of keratinocytes through promoting the transcription of β-catenin/TCF-complex downstream genes.
期刊：
International Journal of Clinical and Experimental Medicine,2020年13(2):574-581 ISSN：1940-5901
通讯作者：
Huang, Yuxiang
作者机构：
[Huang, Yuxiang; Tang, Jianghong] Hunan Univ Chinese Med, Affiliated Hosp 2, Spinal Surg, 230 Cai E North Rd, Changsha 410000, Hunan, Peoples R China.;[Zhu, Shilin] Hunan Univ Tradit Chinese Med, Affiliated Hosp 2, Dept Nursing, Changsha, Hunan, Peoples R China.
通讯机构：
[Huang, Yuxiang] H;Hunan Univ Chinese Med, Affiliated Hosp 2, Spinal Surg, 230 Cai E North Rd, Changsha 410000, Hunan, Peoples R China.
关键词：
Spinal tuberculosis;surgery;collaborative nursing model;compliance;pain;quality of life
摘要：
Objective: This study was designed to analyze the effect of collaborative nursing model on patients after a surgery for spinal tuberculosis. Methods: 93 patients diagnosed with spinal tuberculosis in our hospital from January 2017 to January 2019 were included as the study objects, retrospectively analyzed and randomized into 2 groups. The observation group (n=47) was postoperatively nursed by the collaborative nursing model while the control group (n=46) was routinely nursed. The 2 groups were compared for off-hospital compliance, pain intensity and quality of life (Q0L). Results: (1) The composition ratios of good, intermediate and low off-hospital medication compliance were 42.55%, 48.94% and 8.51% in the observation group, 21.74%, 41.30% and 36.96% in the control group (P<0.05); (2) The complete and partial compliance rates, and noncompliance rate for off-hospital functional exercise were 38.30%, 42.55% and 19.15% in the observation group, 17.39%, 39.13% and 43.48% in the control group (P<0.05); (3) Compared with the control group, the observation group was lower in VAS scores for pains from 1 month to 6 months after surgery (P<0.05), higher in MBI scores for activity of daily living at 1 month, 3 months and 6 months after surgery (P<0.05), and scores of general health (GH), mental health (MH), physical functioning (PF), role emotional (RE), role physical (RP), body pain (BP), social function (SF) and vitality (VT) 3 months after discharge (P<0.05). Conclusion: the application of collaborative nursing model in postoperative nursing patients subject to a surgery for spinal tuberculosis can markedly improve their compliance and quality with alleviated pain intensity after discharge, showing favorable application values.
摘要：
Purpose: To investigate the effect of epigallocatechin gallate (EGCG) on microRNAs in a mouse model of glucocorticoid-induced osteoporosis (GIOP), and the mechanism involved.
Methods: Osteoclast-specific marker mRNA expressions, receptor activator of nuclear factor kappa-B ligand (RANKL), receptor activator of nuclear factor κ B (RANK), and miRNA expressions were determined using reverse transcription polymerase chain reaction (RT-qPCR) analysis. Western blotting was used to assay protein expressions, while miRNA and 3’UTR interaction studies were carried out with reporter assay.
Results: Treatment with EGCG resulted in downregulation of glucocorticoid-induced expressions of RANKL, RANK and osteoclast-specific markers i.e. tumor necrosis factor receptor-associated factor 6, (TRAF6), nuclear factor of activated T cells 1 (NFATc1), cathepsin K, matrix metallopeptidase 9 (MMP9) and tartrate-resistant acid phosphatase (TRAP). Furthermore, EGCG treatment significantly reduced reactive oxygen species (ROS) levels and inflammatory cytokine expressions in GIOP mice. The expression of miRNA-targeting osteoclast marker mmu-mir-193-3p was significantly down-regulated in GIOP mice. However, EGCG treatment increased mmu-mir-193-3p expression and had specific interaction with NFATc1 3’UTR (3’-untranslated region). In vitro results showed that mmu-mir-193-3p mimics downregulated dexamethasone (DXM)-induced osteoclast-specific marker expressions.
Conclusion: These results show that EGCG exerts a protective role against GIOP by upregulating miR- 193a-3p expressions.
Keywords: Epigallocatechin gallate, Glucocorticoids, RANKL, Osteoporosis
作者机构：
[Zhang, Lin; Yang, Hui] Guizhou Univ Tradit Chinese Med, Affiliated Hosp 2, Dept Neurol, Guiyang 550003, Peoples R China.;[Li, Wen-Juan] Hunan Univ Traditional Chinese Med, Changsha 410007, Peoples R China.;[Liu, Ye-Hui] Hunan Univ Tradit Chinese Med, Affiliated Hosp 2, Dept Neurol, 233 CaiE North Rd, Changsha 410005, Hunan, Peoples R China.
通讯机构：
[Liu, Ye-Hui] H;Hunan Univ Tradit Chinese Med, Affiliated Hosp 2, Dept Neurol, 233 CaiE North Rd, Changsha 410005, Hunan, Peoples R China.
关键词：
Ischemic stroke;MALAT1;miR-126;PI3K/AKT
摘要：
Ischemic stroke (IS) is a common disease that seriously endangers human health. Patients with IS present with increased death of brain microvascular endothelial cells (BMECs). MALAT1 is found to be upregulated in IS patients. However, the function of MALAT1 in IS pathogenesis still remains unclear. This study aimed to investigate the role of MALAT1 in IS in vitro model and the related molecular mechanisms. The expressions of MALAT1 and miR-126 were detected by qPCR. The in vitro IS model was established by treating BMECs with oxygen-glucose deprivation (OGD). Cell viability and cell apoptosis were assessed by MTT assay and flow cytometry, respectively. Luciferase assay was conducted to examine the interplay between MALAT1 and miR-126. Western blotting was used to determine the protein levels of apoptosis-associated proteins (e.g. caspase 3, Bax and Bcl-2) and PI3K/Akt pathway-related proteins (e.g. PI3K, Akt, p-PI3K, p-Akt). OGD induced upregulation of MALAT1 and downregulation of miR-126 in HBMECs. MALAT1 knockdown promoted the proliferation of HBMECs and reduced the proportion of apoptotic HBMECs by regulating the expression of apoptosis-related proteins. MALAT1 targeted and negatively regulated miR-126 expression. Overexpression of miR-126 activated the PI3K/Akt pathway, which in turn affected the proliferation and apoptosis of HBMECs. MALAT1 negatively regulated PI3K/Akt pathway. MALAT1 inhibited the proliferation and induced the apoptosis of OGD-induced HBMECs through suppressing PI3K/AKT pathway by sponging miR-126, providing a potential therapeutic target for IS.
