Salicylic acid doped silica nanoparticles as a fluorescent nanosensor for the detection of Fe3+ in aqueous solution.

A novel organic-inorganic hybrid nanosensor (SASP) was prepared by a one-step sol-gel method and characterized by scanning electron microscopy, transmission electron microscopy, Fourier transform infrared spectroscopy, thermogravimetric analysis, N2 adsorption-desorption, fluorescence spectroscopy, etc. The nanosensor showed almost 3-fold fluorescence emission quenching upon excitation with a 293 nm wavelength in the presence of 20 µM Fe3+ ions. The presence of 18 other metal ions had no observable effect on the sensitivity and selectivity of the nanosensor. A fluorescence analysis method based on the SASP for the selective detection of Fe3+ was established under optimal conditions. The results showed that there was a linear relationship between the log luminescence value and the concentration of Fe3+ over the range of 2.0 × 10-7-9.0 × 10-5 mol L-1 with a detection limit (3σ) of 2.5 × 10-8 mol L-1. Furthermore, the proposed method was successfully applied for the determination of trace Fe3+ in fetal bovine serum without the interference of other molecules and ions. Good recovery (96.5-104.5%) and a relative standard deviation of less than 8.6% were obtained from serum samples spiked with four levels of Fe3+. Additionally, the nanosensor showed a good reversibility; the fluorescence could be switched "off" and "on" in two ways, by adjusting the pH of the solution and adding metal chelating agent EDTA.

Diagnostic value of combined detection of IL-1β, IL-6, and TNF-α for sepsis-induced cardiomyopathy / Valor diagnóstico de la detección combinada de IL-1, IL-6, y TNF-α para la cardiomiopatía inducida por sepsis

Introduction:This study aimed to explore the diagnostic value and the correlation of the combined detection of interleukin-1β (IL-1β), interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α) with sepsis-induced cardiomyopathy (SIC).Patients and methods:Admitted to our hospital from January 2017 to January 2019, 96 patients with SIC (a study group) and 90 patients with sepsis (a control group) were enrolled. The three cytokines were determined and the diagnostic value of their combined detection for SIC was analyzed.Results:The cytokines were remarkably higher in the study group (p<.001). The combined detection of the three had a better diagnostic value for SIC (p<.001). The three cytokines were independent risk factors for the death of patients with SIC.Conclusion:IL-1β, IL-6, and TNF-α in SIC patients rise markedly. The combined detection of the three has a better predictive value for patients with SIC and is closely related to the patients’ prognoses, so it may be crucial in diagnosing and treating the disease. (AU)

Introducción:El objetivo de este estudio fue explorar el valor diagnóstico y la correlación de la detección combinada de interleucina-1β (IL-1β), interleucina-6 (IL-6), y factor de necrosis tumoral-α (TNF-α) con la miocardiopatía inducida por sepsis (CIS).Pacientes y métodos:Ingresados en nuestro hospital entre enero de 2017 y enero de 2019, se incluyó en el estudio a 96 pacientes con CIS (grupo de estudio) y 90 pacientes con sepsis (grupo control). Se determinaron las tres citocinas y se analizó el valor diagnóstico de su detección combinada para CIS.Resultados:Las citocinas fueron marcadamente superiores en el grupo de estudio (p<0,001). La detección combinada de las tres tuvo un mejor valor diagnóstico para CIS (p<0,001). Las tres citocinas fueron factores de riesgo independientes de la muerte de los pacientes con CIS.Conclusión:IL-1β, IL-6, y TNF-α se incrementaron considerablemente en los pacientes de CIS. La detección combinada de los tres valores tiene un mejor valor predictivo para los pacientes con CIS, y está estrechamente relacionada con los pronósticos de los pacientes, lo cual puede ser esencial para diagnosticar y tratar la enfermedad. (AU)

Diagnostic value of combined detection of IL-1ß, IL-6, and TNF-α for sepsis-induced cardiomyopathy.

INTRODUCTION: This study aimed to explore the diagnostic value and the correlation of the combined detection of interleukin-1ß (IL-1ß), interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α) with sepsis-induced cardiomyopathy (SIC). PATIENTS AND METHODS: Admitted to our hospital from January 2017 to January 2019, 96 patients with SIC (a study group) and 90 patients with sepsis (a control group) were enrolled. The three cytokines were determined and the diagnostic value of their combined detection for SIC was analyzed. RESULTS: The cytokines were remarkably higher in the study group (p<.001). The combined detection of the three had a better diagnostic value for SIC (p<.001). The three cytokines were independent risk factors for the death of patients with SIC. CONCLUSION: IL-1ß, IL-6, and TNF-α in SIC patients rise markedly. The combined detection of the three has a better predictive value for patients with SIC and is closely related to the patients' prognoses, so it may be crucial in diagnosing and treating the disease.

Traditional Chinese medicine injection for promoting blood circulation and removing blood stasis in treating angina pectoris of coronary heart disease: A protocol for systematic review and network meta-analysis.

BACKGROUND: As a common cardiovascular disease, the morbidity and mortality of coronary heart disease (CHD) are increasing year by year. In recent years, many RCTs have proved that compared with conventional therapy, the combination of TCMIs for promoting blood circulation and removing blood stasis can improve clinical efficacy. However, there is still a lack of direct comparative study between different kinds of TCMIs. Therefore, based on the NMA, this study compares the curative effects of various TCMIs for promoting blood circulation and removing blood stasis in treating CHD to provide a reference for clinical medication. METHODS: We will search PubMed, Web of Science, Embase, The Cochrane Library, China National Knowledge Infrastructure, The Chongqing VIP Chinese Science and Technology Periodic Database, Wanfang Database, and China Biomedical Literature Database for the randomized controlled trials of Danhong injection, Xuesaitong injection, Dengzhanxixin injection, and Salvianolate injection in the treatment of CHD, and we will also manually retrieve from the following databases: Chinese Clinical Trial Register, conference papers, and unpublished studies or references. According to the pre-established inclusion and exclusion criteria, 2 researchers independently screened the literature, extracted the data, and evaluated the RCTs' quality. The primary outcome indicators are the total effective rate of improving angina pectoris symptoms and electrocardiogram improvement. Secondary indicators were angina pectoris attack frequency, angina pectoris attack time, hemorheology, and inflammatory factor level. And use Stata 16.0 software for mesh meta-analysis. Evidence will be checked using the classification of recommendation, evaluation, development, and evaluation. RESULTS: In this study, from the perspective of different kinds of TCMIs for promoting blood circulation and removing blood stasis, we will compare the curative effects of varying treatment measures and rank the curative effects. CONCLUSION: This study will evaluate the efficacy of different kinds of TCMIs for promoting blood circulation and removing blood stasis in the treatment of CHD and help clinicians improve their clinical effectiveness. UNIQUE INPLASY NUMBER: INPLASY202130103.

Atmospheric fine particulate matter exposure exacerbates atherosclerosis in apolipoprotein E knockout mice by inhibiting autophagy in macrophages via the PI3K/Akt/mTOR signaling pathway.

Fine particulate matter (PM2.5) exposure is intimately linked to atherosclerosis. Defective macrophages autophagy plays an accelerated role in advanced atherosclerosis, however, whether macrophages autophagy has been implicated in the development of PM2.5-induced atherosclerosis has not been analyzed in full detail. Here we aimed to investigate the association between macrophages autophagy and PM2.5-induced atherosclerosis, as well as the underlying mechanisms. ApoE-/- mice were randomly exposed to PM2.5 or filtered air for 3 months, macrophage RAW264.7 cells were isolated and were stimulated with PM2.5 sample, selective inhibitors of PI3K/Akt/mTOR pathway LY294002, triciribine, and rapamycin were used in vitro and in vivo to detect the potential mechanisms. We found that PM2.5 could significantly accelerate atherosclerotic plaque formation in ApoE-/- mice, increase serum levels of TC and LDL-C, accelerate lipid accumulation in RAW264.7 cells, elevate serum and supernatant levels of IL-6, TNF-α and hs-CRP, decrease the number of autophagosomes in aortic plaque and RAW264.7 cells, reduce the expressions of autophagy-related genes LC3-I, LC3-II and Beclin1 in aortic tissues and RAW264.7 cells but increase the expression of autophagy regulator p62, elevate PI3K, Akt and mTOR distributions in aorta, and increase p-PI3K, p-Akt and p-mTOR protein expressions in aorta and RAW264.7 cells. However, these effects of PM2.5 were aggravated with the administration of LY294002, triciribine, or rapamycin. This study indicated that the PI3K/Akt/mTOR pathway is involved in the suppression of autophagy induced by PM2.5 in macrophages, the accelerated effect of PM2.5 on atherosclerosis was mediated by down-regulation of macrophages autophagy via activating the PI3K/Akt/mTOR signaling pathway.

Ambient fine particulate matter aggravates atherosclerosis in apolipoprotein E knockout mice by iron overload via the hepcidin-ferroportin axis.

AIMS: Exposure to fine particulate matter (PM2.5) is correlated to atherosclerosis, but the mechanism remains largely undefined. Iron overload is a significant contributor to atherosclerosis, and iron homeostasis is highly regulated by the hepcidin-ferroportin (FPN) axis. Here we aimed to investigate the association between iron overload and PM2.5-induced atherosclerotic mice. MAIN METHODS: Apolipoprotein E knockout (ApoE-/-) mice were randomly assigned to filtered air (FA group) or PM2.5 (PM2.5 group) for 3-month inhalation. Daily PM2.5 mass concentrations, serum levels of ferritin, iron, pro-atherosclerotic cytokines and lipid profiles, atherosclerotic lesion areas, hepcidin, FPN and iron depositions in atherosclerotic lesions, hepcidin, FPN mRNA and protein expressions in the aorta were detected, respectively. KEY FINDINGS: The daily average concentration of atmospheric PM2.5 was 68.2 ± 21.8 µg/m3. Serum levels of ferritin, iron, VEGF, MCP-1, IL-6, TNF-α, TC and LDL-C, atherosclerotic lesion areas, hepcidin and iron depositions in atherosclerotic lesions, hepcidin mRNA and protein expressions in the PM2.5 group were observably higher than those in the FA group. Nevertheless, FPN deposition in atherosclerotic lesions, FPN mRNA and protein expressions in the aorta of the PM2.5 group were markedly lower than those of the FA group. SIGNIFICANCE: PM2.5 inhalation could exacerbate the formation and development of atherosclerosis in ApoE-/- mice, the potential mechanisms may be partly associated with iron overload via the hepcidin-FPN axis, as well as iron-triggered systemic inflammation and hyperlipidemia.

Regulatory effect of traditional Chinese medicine on gut microbiota in patients with atherosclerosis: A protocol for systematic review and meta-analysis.

BACKGROUND: Atherosclerosis is the pathological basis of many cardiovascular and cerebrovascular diseases, and its pathogenesis is complex. Recent studies revealed a significant role of gut microbiota in the onset and development of atherosclerosis. Traditional Chinese medicine has rich clinical experience and unique advantages in the treatment of atherosclerosis. A large number of studies have proved that traditional Chinese medicine has the functions of reducing blood lipid, regulating gut microbiota, and resisting inflammation. The aim of this systematic review is to observe the randomized controlled trial of traditional Chinese medicine in treating gut microbiota, so as to evaluate the effectiveness and safety of traditional Chinese medicine in treating atherosclerosis patients. METHODS: The English database (PubMed, Web of Science, Embase, the Cochrane Library) and Chinese database (China National Knowledge Infrastructure, the Chongqing VIP Chinese Science, and Technology Periodic Database, Wanfang Database, and China Biomedical Literature Database) will be searched up to October 2020. We will also manually search the Chinese clinical trial register, conference papers, and unpublished studies or references. Randomized control trials of traditional Chinese medicine treatment of atherosclerosis were collected comprehensively, and 2 researchers will independently screen literature, data extraction, and evaluation the quality of literature methodology. The primary outcomes are lipid metabolism and gut microbiota and their metabolites. The secondary outcomes are the change of inflammatory markers. Meta-analysis was performed by RevMan 5.3.5 software. The Grades of Recommendation, Assessment, Development, and Evaluation will be used to evaluate the outcome quality of evidence. RESULTS: This study will comprehensively review the existing evidence of traditional Chinese medicine in treating atherosclerosis from the perspective of gut microbiota. CONCLUSION: This study will provide information on the effectiveness and safety of traditional Chinese medicine in treating atherosclerosis from the perspective of gut microbiota. UNIQUE INPLASY NUMBER: INPLASY2020110056.

Jianpi Huazhuo Tiaozhi granules reduce oxidative stress injury in macrophages by inhibiting the nicotinamide adenine dinucleotide phosphate oxidase/reactive oxygen species-nuclear transcription factor kappa B pathway.

OBJECTIVE: To assess the effect of Jianpi Huazhuo Tiaozhi granules (JHTG) on oxidative stress damage to macrophages and explore the relationship between the levels of this damage and the nicotinamide adenine dinucleotide phosphate oxidase (NOX)/reactive oxygen species (ROS)- nuclear transcription factor kappa B (NF-κB) signaling pathway. METHODS: Macrophages cultured in vitro were divided into seven groups: control, model control, inhibitor, positive control, 2.5% JHTG, 5% JHTG, and 10% JHTG. An oxidative stress injury model was established by stimulating macrophages with oxidized low-density lipoprotein. Cell survival and apoptosis were detected by 3-(4,5)-dimethylthiahiazo (-z-y1)-3,5-di- phenytetrazoliumromide and flow cytometry assays, respectively. Malondialdehyde and superoxide dismutase levels were detected by enzyme-linked immunosorbent assays, while ROS levels were detected using a fluorescence probe. Proteins and mRNAs associated with the NOX/ROS-NF-κB pathway, including NOX4, p22phox, inhibitor of NF-κB kinase-α (IKK-α), inhibitor of NF-κB kinase-ß (IKK-ß), and NF-κB were detected by Western blot and PCR, respectively. RESULTS: After JHTG treatment, there were fewer damaged and apoptotic macrophages, while superoxide dismutase levels were elevated. The JHTG-treated groups also showed reduced ROS levels. The molecular changes following JHTG treatment included decreased expression of NOX4 and p22phox at the protein level and decreased IKK-α, IKK-ß, and NF-κB expression at the mRNA level. All of these effects were correlated with the JHTG concentration. CONCLUSION: These results demonstrated that the molecular mechanism underlying the antioxidant activity of JHTG in macrophages is through inhibiting the NOX/ROS-NF-κB pathway.

Qishen Yiqi dripping pills for chronic ischaemic heart failure: results of the CACT-IHF randomized clinical trial.

AIMS: Qishen Yiqi dripping pills (QSYQ) may be beneficial in patients with ischaemic heart failure (IHF). We aimed to assess the efficacy and safety of QSYQ administered together with guideline-directed medical therapy in patients with IHF. METHODS AND RESULTS: This prospective randomized, double-blind, multicentre placebo-controlled study enrolled 640 patients with IHF between March 2012 and August 2014. Patients were randomly assigned to receive 6 months of QSYQ or placebo in addition to standard treatment. The primary outcome was 6 min walking distance at 6 months. Among the 638 IHF patients (mean age 65 years, 72% men), the 6 min walking distance increased from 336.15 ± 100.84 to 374.47 ± 103.09 m at 6 months in the QSYQ group, compared with 334.40 ± 100.27 to 340.71 ± 104.57 m in the placebo group (mean change +38.32 vs. +6.31 m respectively; P < 0.001). The secondary outcomes in composite clinical events, including all-cause mortality and emergency treatment/hospitalization due to heart failure, were non-significantly lower at 6 months with QSYQ compared with placebo (13% vs. 17%; P = 0.45), and the change of brain natriuretic peptide was non-significantly greater with QSYQ compared with placebo (median change -14.55 vs. -12.30 pg/mL, respectively; P = 0.21). By contrast, the Minnesota Living with Heart Failure Questionnaire score significantly improved with QSYQ compared with placebo (-11.78 vs. -9.17; P = 0.004). Adverse events were minor and infrequent with QSYQ, similar to the placebo group. CONCLUSIONS: Treatment with QSYQ for 6 months in addition to standard therapy improved exercise tolerance of IHF patients and was well tolerated.

Honokiol Suppressed Pancreatic Cancer Progression via miR-101/Mcl-1 Axis.

BACKGROUND: Pancreatic cancer is one of the most aggressive malignancies. The present study aimed to examine the anti-tumor effects of honokiol in pancreatic cancer and to explore the underlying molecular mechanisms. MATERIALS AND METHODS: In vitro functional assays determined pancreatic cancer cell proliferation, apoptosis and invasion. Xenograft nude mice model determined the in vivo anti-cancer effects of honokiol. Luciferase reporter assay determined the interaction between miR101 and myeloid cell leukemia-1 (Mcl-1). RESULTS: Honokiol concentration-dependently suppressed pancreatic cancer cell viability. In addition, honokiol increased the caspase-3 activity and cell apoptotic rates, induced cell cycle arrest at G0/G1 phase, and inhibited cell invasion in pancreatic cancer. Interestingly, honokiol treatment induced up-regulation of miR-101 in pancreatic cancer cells. Knockdown of miR-101 attenuated the honokiol-induced cell apoptosis and inhibition in cell invasion of pancreatic cancer cells. On the other hand, miR-101 overexpression induced cell apoptosis and inhibited cell viability and invasion in pancreatic cancer. Further mechanistic study verified that Mcl-1 was negatively regulated by miR-101, and Mcl-1 overexpression counteracted the tumor-suppressive effects of honokiol on the pancreatic cancer cells. In vivo studies showed that honokiol dose-dependently suppressed tumor growth of pancreatic cancer in the nude mice and up-regulated miR-101 expression but down-regulated Mcl-1 expression in tumor tissues. CONCLUSION: Our data showed that honokiol suppressed pancreatic cancer progression via miR-101-Mcl-1 axis. Honokiol could be a promising candidate for cancer prevention and/or therapeutic treatment for pancreatic cancer.

Effect and safety of acupotomy in treatment of knee osteoarthritis: a systematic review and Meta-analysis.

OBJECTIVE: To evaluate the clinical efficacy and safety of acupotomy in treatment of knee osteoarthritis (OA). METHODS: Extensive literature searches were carried out in PubMed, EMBASE, Cochrane Library (Issue 5, 2017), Chinese Biomedical Literature Database, China National Knowledge Infrastructure Database, China Science and Technology Journal Database and Wanfang Database. All databases were retrieved from their inception until May 31, 2017. Randomized controlled trials incorporating acupotomy versus intra-articular sodium hyaluronate for knee osteoarthritis were included. According to Cochrane Reviews' Handbook (5.2), two reviewers screened each article and extracted data independently and were blinded to the findings of each reviewer. Meta-analysis was performed by the Cochrane Collaboration's RevMan 5.3 software. RESULTS: We identified 12 studies involving 1150 patients aged between 40 and 78 years old. The pooled analysis indicated that acupotomy showed a significant improvement for short-term effect [cure rate: odds ratio (OR) = 2.04, 95% confidence interval (CI) (1.46, 2.85), P < 0.01; total effective rate: OR = 2.25, 95% CI (1.55, 3.28), P < 0.01; pain score: standard mean difference (SMD) = －1.02; 95% CI (－1.72, －0.31); P = 0.005; Western Ontario and McMaster Universities Questionnaire (WOMAC) score: SMD = －0.74; 95% CI (－1.11, －0.37); P < 0.01]; and also for long-term effect [total effective rate: OR = 2.99, 95%CI (1.88, 4.76), Z = 4.64, P < 0.01; pain score: SMD = －1.68; 95% CI (－2.14, －1.22); P < 0.001; WOMAC score: SMD = －0.91; 95% CI (－1.40, －0.41); P < 0.001]. In addition, there was no obvious difference between acupotomy group and control group in adverse events [OR = 2.13, 95%CI (0.14, 32.28), P = 0.58]. CONCLUSION: Acupotomy is a safe and effective treatment for KOA. However, due to the methodological deficiency of the included studies, well-designed randomized controlled trials are required to further confirm the findings.

Triptolide ameliorates fine particulate matter-induced podocytes injury via regulating NF-κB signaling pathway.

BACKGROUND: PM2.5 is associated closely with an increased risk of membranous nephropathy (MN), however, whether PM2.5 could induce podocytes injury, the underlying pathology for MN, has not be thoroughly studied. Triptolide, an active component in Tripterygium wilfordii Hook F, is frequently used to treat MN in China, but its effects on PM2.5-induced podocytes injury is still largely unknown. Therefore, we evaluated the effects of PM2.5 on podocytes, and explored whether triptolide could improve PM2.5-induced podocytes injury and the possible underlying mechanisms. RESULTS: Podocytes were incubated with PM2.5 after being pre-treated with triptolide, viability, apoptosis rate and migratory capacity of podocytes were determined by CCK-8 assay, flow cytometry and Transwell assay, respectively. Additionally, the levels of lactate dehydrogenase (LDH), malondialdehyde (MDA), and superoxide dismutase (SOD) in podocytes, the cytoskeleton of podocytes, the protein expressions of nephrin, podocin, Bcl-2, Bax, nuclear factor kappa-B/p65 (NF-κB/p65) and phospho-inhibitor of NF-κB (p-IκBα) were measured. Our data showed that PM2.5 treatment significantly increased the disorganization of F-actin stress fibers, the damaged structural integrity of nucleus, the deranged and dissociated cytoskeleton in podocytes, increased the podocytes apoptosis rate, the levels of MDA and LDH, markedly up-regulated the protein expression of Bax, NF-κB/p65 and p-IκBα, down-regulated the protein expression of nephrin, podocin and Bcl-2, and significantly decreased the level of SOD, the migration rate and the viability of podocytes, compared with those of the untreated podocytes. These effects of PM2.5 on podocytes, however, were reversed by triptolide administration. CONCLUSION: These results suggest that triptolide could prevent against PM2.5-induced podocytes injury via suppressing NF-κB signaling pathway.

Acceleratory effects of ambient fine particulate matter on the development and progression of atherosclerosis in apolipoprotein E knockout mice by down-regulating CD4+CD25+Foxp3+ regulatory T cells.

OBJECTIVE: Atherosclerosis is an autoimmune inflammatory disease that is closely associated with long-term exposure to fine particulate matter (PM2.5). CD4+CD25+Foxp3+ regulatory T cells (Tregs) play a critical role in the regulation of T cell-mediated immune responses, and the depletion of CD4+CD25+Foxp3+ Tregs has been thought to play a prominent role in atherosclerosis. Therefore, we investigated the association between the CD4+CD25+Foxp3+ Tregs population and atherosclerotic development in ApoE-/- mice exposed to PM2.5. METHODS: We employed a real-world system to subject 40 ApoE-/- mice to ambient inhalation of PM2.5 (PM2.5 group, n = 20) or filtered air (FA group, n = 20) for 12 weeks. PM2.5 source apportionment, atherosclerotic lesions within aorta, lipid deposition and plaque accumulation in whole artery, serum level of inflammatory factors and lipid profiles, CD4+CD25+Foxp3+ Tregs population in splenocytes, Foxp3 protein and mRNA expressions in descending aorta and spleen were quantified, respectively. RESULTS: The daily average concentration of PM2.5 was 57.4 ± 25.6 µg/m3. Atherosclerotic lesions within aorta, lipid deposition and plaque accumulation in whole artery, serum levels of IL-6, TNF-α, TC and LDL-C in the PM2.5 group increased significantly compared to the FA group. Whereas, serum levels of IL-10 and TGF-ß, CD4+CD25+Foxp3+ Tregs population in splenocytes, Foxp3 protein and mRNA expressions in descending aorta and spleen in the PM2.5 group decreased significantly compared to the FA group. CONCLUSION: These results suggest that PM2.5 could accelerate the development of atherosclerosis in ApoE-/- mice, which is related to CD4+CD25+Foxp3+ Tregs down-regulation, as well as lipid deposition and systemic inflammation.

Detoxification and activating blood circulation decoction reduces restenosis involving the TLR4/NF-κB pathway after balloon injury.

Restenosis is a major problem after percutaneous coronary intervention (PCI) treatment. Inflammation is one of the major core mechanisms involved in the occurrence of restenosis, and plays an important role in intimal hyperplasia. Detoxification and activating blood circulation decoction (DABCD) is a traditional Chinese medicine that is used in the treatment and prevention of atherosclerotic and inflammatory diseases. Our previous studies demonstrated that DABCD-mediated cardioprotection involves anti-inflammatory mechanisms and could be developed as a novel drug for the treatment of vascular smooth muscle cell (VSMC) proliferation and aortic restenosis. A rat model of postoperative restenosis after PCI was generated by balloon injury to determine the protective effects and potential mechanisms of DABCD. The injured segments of aortae were collected on days 14 and 28 after the operation to observe the morphological changes in the vascular structure and measure the proportion of inflammatory factors in plasma and vascular tissues, as well as test the proliferative activity of VSMCs. The expression of related proteins, namely, Toll-like receptor (TLR) 4 and nuclear factor (NF)-κB, in the mechanistic study was clarified by western blot analysis. We tested the hypothesis that the cardioprotective effects of DABCD on aortic restenosis are associated with the inhibition of aortic intimal hyperplasia in this model. Our results showed that DABCD has protective effect on rat aortic restenosis and the anti-inflammatory mechanism of DABCD on balloon-induced restenosis in rat may be due to its ability to inhibit TLR4-mediated NF-κB signaling pathways. DABCD may be a potential therapeutic agent against restenosis.

Acupotomy Therapy for Shoulder Adhesive Capsulitis: A Systematic Review and Meta-Analysis of Randomized Controlled Trials.

OBJECTIVE: Acupotomy therapy is widely used for pain management. However, the efficacy of acupotomy on shoulder adhesive capsulitis (SAC) is still uncertain. The aim of this study was to determine the effectiveness and safety of acupotomy therapy for SAC. METHODS: We searched seven electronic databases to collect randomized controlled trials (RCTs) of acupotomy for SAC published before April 2019. A meta-analysis was performed according to the Cochrane systematic review method by using RevMan 5.3 software. RESULTS: A total of eight RCTs involving 501 patients were enrolled. Meta-analysis showed that acupotomy was significantly better than the control group in debasing the Visual Analogue Scale (VAS) score (MD = -0.97, 95% CI = [-1.49, -0.45], P=0.0003) and improving the Constant-Murley Score (CMS) (MD = 8.46, 95% CI = [1.04, 15.87], P=0.03), and there was no significant difference in adverse events (OR = 1.24, 95% CI = [0.34, 4.52], P=0.74) between the two groups. CONCLUSION: Acupotomy therapy is an effective and safe treatment for SAC, and this treatment can be recommended for the management of SAC. Due to the low quality and small sample size of the included studies, more rigorously designed RCTs with high quality and large-scale are recommended in future.

Association of Depression/Anxiety Symptoms with Neck Pain: A Systematic Review and Meta-Analysis of Literature in China.

Background: Due to its high morbidity and prevalence, the potential relationships of depression/anxiety symptoms in neck pain (NP) are not well demonstrated. Objectives: This study aimed to conduct a comprehensive estimation of controlled trials of psychological problems and to test hypotheses concerning whether NP was statistically relative to anxiety/depression symptoms. Methods: Chinese literature databases such as the China National Knowledge Infrastructure (CNKI), VIP Information (VIP), Chinese Biomedicine (CBM), and Wanfang Data (WANFANG) were scientifically searched for reports published until February 5, 2018. Controlled trials incorporating NP patients with anxiety/depression versus healthy people were contained. Two researchers screened each article and extracted data, respectively, and blinded to the findings of each other. Meta-analysis was conducted by the Cochrane Collaboration's RevMan 5.3 and Stata 14.0 (Stata Corp LP, USA) software. Results: We identified 13 eligible studies involving 2339 patients and 3290 healthy people. Compared with healthy control participants, the findings indicated that depression/anxiety symptoms were more common or severe in NP patients (respectively, SMD = 0.89; 95% CI = (0.58, 1.20); P < 0.01 and SMD = 0.92; 95% CI = (0.65, 1.20); and P < 0.01), results from the pooled data demonstrated no statistical significance between depression/anxiety symptoms and gender in NP patients (resp., SMD = 0.16; 95% CI = (-0.18, 0.51); P=0.35 and SMD = -0.08; 95% CI = (-0.42, 0.27); and P=0.67), and the combined data of the incidence of depression or anxiety symptoms revealed significant difference between NP patients and healthy persons (resp., RR = 4.81; 95% CI = (3.30, 7.01); P < 0.01 and RR = 3.29; 95% CI = (2.16, 5.00); and P < 0.01). In addition, we did not find articles that met the inclusion criteria, which compared NP patients with other physical illnesses in terms of anxiety/depression symptoms. Conclusions: This meta-analysis suggests that anxiety/depression symptoms are associated with high morbidity in NP patients. We consider these reports support the viewpoint that nonspecific mechanisms mediate mental disturbances in NP. This study may have clinical value for NP, offering an underlying target for the prevention and treatment of anxiety/depression.

Puerarin inhibits vascular smooth muscle cells proliferation induced by fine particulate matter via suppressing of the p38 MAPK signaling pathway.

BACKGROUND: Fine particulate matter (PM2.5) is a major risk factor for the development and progression of atherosclerosis. Proliferation and infiltration of vascular smooth muscle cells (VSMCs) from the blood vessel media into the intima is a crucial step in the pathophysiology of atherosclerosis. Puerarin, a natural extract from Radix Puerariae, possesses significant anti-atherosclerosis properties. However, the underlying molecular mechanisms responsible for the effect of puerarin on the VSMCs proliferation induced by PM2.5 remain unclear. The present study was designed to examine the effect of puerarin on PM2.5-induced VSMCs proliferation, and to explore the p38 mitogen-activated protein kinase (p38 MAPK) signal mechanism involved. METHODS: VSMCs viability was measured by CCK-8 assay, VSMCs proliferation was assessed by BrdU immunofluorescence, the levels of superoxide dismutase (SOD) and malonaldehyde (MDA) were assayed by colorimetric assay kits, the levels of nitric oxide (NO) and endothelin-1 (ET-1) were determined by nitrate reductase method and radioimmunoassay, the levels of vascular cell adhesion molecule-1 (VCAM-1), interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α) were measured by ELISA. The protein expressions of phospho-p38 MAPK (p-p38 MAPK) and proliferating cell nuclear antigen (PCNA) in the VSMCs were subjected by Western blot. RESULTS: Compared to the PM2.5-treated cells, in addition to inhibiting the PM2.5-induced VSMCs proliferation, puerarin also down-regulated the protein expressions of p-p38 MAPK and PCNA, decreased the levels of ET-1, VCAM-1, IL-6, TNF-α and MDA, increased the levels of NO and SOD. Moreover, the anti-proliferative effects of puerarin were significantly enhanced by the co-incubation of puerarin with SB203580, a selective inhibitor of p38 MAPK, as compared to the puerarin-treated cells. CONCLUSION: These results suggest that puerarin might suppress the PM2.5-induced VSMCs proliferation via the inhibition of the p38 MAPK signaling pathway.

Suppressive effects of berberine on atherosclerosis via downregulating visfatin expression and attenuating visfatin-induced endothelial dysfunction.

Berberine (BBR) possesses significant anti-atherosclerosis properties. Visfatin is one of the most promising biomarkers of incoming atherosclerosis. However, research on the effect of BBR on regulating visfatin expression in atherogenesis remains largely unknown. In this study, we investigated the effects of BBR on visfatin expression and atherogenesis in apolipoprotein E knockout (ApoE-/-) mice. The effect of BBR on attenuating visfatin-induced endothelial dysfunction was also evaluated in cultured human umbilical vein endothelial cells (HUVECs). In vivo experiments showed that BBR treatment (5 mg/kg/day) significantly reduced the serum levels of visfatin, lipid, interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α), the protein expression of visfatin, p-p38 MAPK and p-c-Jun N-terminal kinase (JNK) in mice aorta and the distribution of visfatin in the atherosclerotic lesions in ApoE-/- mice fed with a Western diet. In addition, in vitro experiments indicated that visfatin (100 µg/l) significantly increased apoptosis, the contents of IL-6 and TNF-α, the protein levels of p-p38 MAPK, p-JNK and Bax in HUVECs, which were reversed by BBR administration (50 µmol/l). Our findings suggest that BBR significantly ameliorates Western diet-induced atherosclerosis in ApoE-/- mice via downregulating visfatin expression, which is related to the inhibition of p38 MAPK and JNK signaling pathways and subsequent suppression of visfatin-induced endothelial dysfunction.

Multiplex TaqMan locked nucleic acid real-time PCR for the differential identification of various meat and meat products.

Meat adulteration incidents have been reported frequently over the past few years, and the corresponding traceability issues attracted much more attention due to the customer's demands and administration's responsibility. Therefore, it is important to develop high-throughput and rapid detection methods to identify the specific sources from meat samples. In this study, a multiplex TaqMan locked nucleic acid real-time polymerase chain reaction assay (MLNA-RT-PCR) was developed to simultaneously detect multiple meat sources (duck, pork, beef and chicken). PCR primers and TaqMan-LNA probes were designed based on species-specific mitochondrial gene sequences, and the MLNA-RT-PCR was developed and optimized for better performance. The specificity of this assay was verified through identifying unrelated (sheep, horse, deer, donkey, rabbit, goose, goat, shrimp, salmon and maize) mitochondrial DNA as species-specific targets. The detection limit for MLNA-RT-PCR reached to the level of 0.01% of each species. The assay was then used to identify the meat sources of commercial meat and meat-derived products that were obtained from markets in Shantou, and the results were 98% consistent with that obtained from detection based on the national standard. In conclusion, this MLNA-RT-PCR is a high-throughput, sensitive and specific method that can be used to identify multiple meat sources in meat and meat-derived products.

[Study of Berberine on Attenuating PM2.5-Induced Vascular Endothelial Cells Injury by ERK1/2 Signal Pathway].

Objective: To investigate the effect and mechanism of berberine in attenuating PM2. 5-induced human umbilical vein endothelial cells EA. hy926 injury. Methods: The samples of fine particulate matter( PM2. 5) were collected and made into suspension. Different concentrations of PM2. 5( 0,20,200,400 mg / L) were added into EA. hy926 cells for 24 h. The viability of EA. hy926 cells was detected by MTT assay, and apoptosis of EA. hy926 cells was detected by flow cytometry, the expressions of p-ERK1 /2,BAX and BCL-2 in the EA. hy926 cells were measured by Western blot,the contents of IL-6,TNF-α were measured by ELISA, the content of MDA, and the activities of SOD and LDH in the EA. hy926 cells culture supernatant were measured, respectively. Different concentrations of berberine( 10,50,100 µmol / L) and PD98059( 20 µmol / L) was added into the EA. hy926 cells to observe the effect of berberine. Results: Compared with control group,PM2. 5 decreased the viability in a dose dependent manner, and significantly upgraded the protein levels of p-ERK1 /2 and BAX / BCL-2 ratio,PM2. 5 increased the apoptosis of EA. hy926 cells, and increased the contents of IL-6,TNF-α and MDA, increased the activity of LDH, and decreased SOD activity in the EA. hy926 cells( P < 0. 05). Compared with PM2. 5 group, berberine increased the viability of EA. hy926 cells in a dose dependent manner,PM2. 5 significantly downgraded the protein levels of p-ERK1 /2 and BAX / BCL-2 ratio, and decreased the apoptosis of EA. hy926 cells, decreased the contents of IL-6,TNF-α and MDA, and decreased the activity of LDH, and increased SOD activity in the EA. hy926 cells( P < 0. 05). Conclusion: Berberine attenuates PM2. 5-induced EA. hy926 cells injury by inhibiting ERK1 /2 pathway.