Effects of different parameters of Tai Chi on the intervention of chronic low back pain: A meta-analysis.

OBJECTIVE: To evaluate the effects of Tai Chi in the treatment of patients with chronic low back pain by Meta-analysis and to investigate its influencing factors. METHODS: The study searched eight databases (PubMed, Embase, The Cochrane Library, Web of Science, China Knowledge Network, Wanfang, VIP, and CBM) from inception to October 2023. Two investigators independently selected 10 eligible randomized controlled trials (RCT) against inclusion and exclusion criteria, followed by data extraction and study quality assessment by ROB 2. The outcomes of interest were pain intensity and disability. The studies were combined using meta-analysis when statistical pooling of data was possible. The quality of the evidence was assessed using the GRADE approach. RESULTS: 10 randomized controlled studies with a total sample of 886 cases were included, of which 4 (40%) were assessed as low risk of bias. The effect size of Tai Chi for chronic low back pain was [Weighted Mean Difference (WMD) with 95% Confidence Interval (CI) = -1.09 (-1.26, -0.92), p < 0.01], all achieving large effect sizes and statistically significant; the effect size for disability was [Standard Mean Difference (SMD) with 95% CI = -1.75 (-2.02, -1.48), p < 0.01], and the combined effect sizes of physical health and mental health for quality of life were [WMD (95% CI) = 4.18 (3.41, 4.95), p < 0.01; WMD (95% CI) = 3.23 (2.42, 4.04), p < 0.01] respectively. The incidence of adverse reactions was low. Meta regression and subgroup analysis showed that there was no significant effect on intervention measures (Tai Chi alone, Tai Chi as additional therapy, water Tai Chi), Tai Chi school (Chen and Yang) and the number of total intervention sessions (> 30 and ≤ 30). The evidence quality evaluation showed that the evidence of pain, physical health of quality of life and mental health score was medium quality, while the evidence of disability and adverse reactions was low quality. CONCLUSIONS: Tai Chi has an obvious effect of in relieving chronic low back pain. Tai Chi alone and Tai Chi as supplementary therapy have good effects. Tai Chi in water have not been verified. Chen style Tai Chi and Yang's Tai Chi, intervention more than 30 times or less than 30 times had no significant difference in the effect of intervention on CLBP.

The role of mitophagy in metabolic diseases and its exercise intervention.

Mitochondria are energy factories that sustain life activities in the body, and their dysfunction can cause various metabolic diseases that threaten human health. Mitophagy, an essential intracellular mitochondrial quality control mechanism, can maintain cellular and metabolic homeostasis by removing damaged mitochondria and participating in developing metabolic diseases. Research has confirmed that exercise can regulate mitophagy levels, thereby exerting protective metabolic effects in metabolic diseases. This article reviews the role of mitophagy in metabolic diseases, the effects of exercise on mitophagy, and the potential mechanisms of exercise-regulated mitophagy intervention in metabolic diseases, providing new insights for future basic and clinical research on exercise interventions to prevent and treat metabolic diseases.

The roles of ubiquitination and deubiquitination of NLRP3 inflammasome in inflammation-related diseases: A review.

The inflammatory response is a natural immune response that prevents microbial invasion and repairs damaged tissues. However, excessive inflammatory responses can lead to various inflammation-related diseases, posing a significant threat to human health. The NOD-like receptor pyrin domain-containing protein 3 (NLRP3) inflammasome is a vital mediator in the activation of the inflammatory cascade. Targeting the hyperactivation of the NLRP3 inflammasome may offer potential strategies for the prevention or treatment of inflammation-related diseases. It has been established that the ubiquitination and deubiquitination modifications of the NLRP3 inflammasome can provide protective effects in inflammation-related diseases. These modifications modulate several pathological processes, including excessive inflammatory responses, pyroptosis, abnormal autophagy, proliferation disorders, and oxidative stress damage. Therefore, this review discusses the regulation of NLRP3 inflammasome activation by ubiquitination and deubiquitination modifications, explores the role of these modifications in inflammation-related diseases, and examines the potential underlying mechanisms.

Effects of Tai Chi on Sleep Quality as Well as Depression and Anxiety in Insomnia Patients: A Meta-Analysis of Randomized Controlled Trials.

To systematically review the effects of Tai chi on sleep quality, depression, and anxiety in patients with insomnia. The electronic databases including PubMed, Cochrane Library, Web of Science, Embase, China National Knowledge Infrastructure (CNKI), WanFang Data, Chinese Biomedical Literature Database (CBM), and VIP Database for Chinese Technical Periodicals (VIP) were retrieved and screened by computer. Randomized controlled trials (RCT) on patients with insomnia who practiced Tai chi were collected, and the RCT risk of bias assessment criteria was used to evaluate the methodological quality of the included studies. The combined effect size was expressed as the weighted mean difference (WMD), with a confidence interval of 95% (CI). Review Manager 5.4 and Stata16.0 were used for heterogeneity analysis and sensitivity analysis. Tai chi reduced the patients' Pittsburgh sleep quality index (PSQI) score (WMD = -1.75, 95% CI: -1.88, -1.62, p < 0.001); Hamilton depression scale (HAMD) score (WMD = -5.08, 95% CI: -5.46, -4.69, p < 0.001), Hamilton anxiety scale (HAMA) score (WMD = -2.18, 95% CI: -2.98, -1.37, p < 0.001), and self-rating anxiety scale (SAS) score (WMD = -7.01, 95% CI: -7.72, -6.29, p < 0.001). Tai chi exercise has a good preventive and ameliorating effect on insomnia, which can relieve patients' depression and anxiety, simultaneously enhancing various functions of the body. However, most of the included studies reported random assignment with some lack of specific descriptions, and the blinding of participants was difficult to achieve due to the nature of exercise, which may cause bias. Therefore, more high-quality, multi-center, and bigger-sample studies need to be included in the future to further verify the results.

Policy Analysis of the Integration of Sports and Medicine against the Backdrop of "Healthy China": A Qualitative Study Using NVivo.

In China, the aim of integrating sports and medicine is part of a national health promotion policy. It is important to clarify the relevant policy points, policy practice distribution, and practical tools, as well as to find the weak links in the policy. In the study, there are 34 primary child nodes, 12 secondary child nodes and four parent nodes that were formed. In this study NVivo 11 software was used to analyze the content of 15 national guidelines in terms of integrating sports and medicine. From 2014 to 2021, the policy development of the integration of sports and medicine went through the beginning and growth stages. The evolutionary logic presents an inverse relationship between the policy practice's duration and the degree of state intervention. In the sequential developmental phases, policy tools were set up in an orderly transition from a single mandatory policy tool to a voluntary or hybrid policy tool, supplemented by essential policy tools. With respect to the policy content, the attention to specific service groups and sports risk assessment is insufficient. In the future, we should actively focus on the division of particular service groups and their service supply, pay closer attention to the social needs and value manifestation of sports risk assessment, and balance the proportion of policy tools in the development of the integration of sports and medicine.

Effects of isometric training on the treatment of patients with neck pain: A meta-analysis.

BACKGROUND: The aim of this meta-analysis was to evaluate the effects of isometric training interventions on the treatment of patients with neck pain. METHODS: Electronic databases, including PubMed, The Cochrane Library, Web of Science, etc., were retrieved and screened by computer, and 18 articles with a total of 868 samples were included. Review Manager 5.4 software was used for the meta-analysis. RESULTS: The meta-analysis results showed that isometric training can reduce visual analogue scale scores of patients[weighted mean difference (95% confidence interval) = -0.80(-0.88, -0.73), P < .00001]; decrease patients neck disability index score, isometric training was better than the control group [weighted mean difference (95% confidence interval) = 5.55 (4.57, 6.53), P < .0001]; in improving patients' motion of the sagittal plane [weighted mean difference (95% confidence interval) = 1.53 (-0.40, 3.63), P = .12], coronal plane [weighted mean difference (95% confidence interval) = 2.12 (0.56, 3.68), P = .008], horizontal plane [weighted mean difference (95% confidence interval) = 3.58 (1.56, 5.59), P = .0005], isometric training was superior to the control group. More than 20 isometric training interventions had more significant effects on visual analogue scale and range of motion. And isometric training for more than 8 weeks had more significant effects on the visual analogue scale and neck disability index scores. CONCLUSION: Isometric training has significant effects on relieving neck pain, improving neck dysfunction, and improving joint mobility. However, the two indicators of visual analogue scale and neck disability index had more influential factors; the sample size of most studies was relatively small, and the intervention measures in the control group were relatively simple. It is expected that more abundant research will expand and deepen in the future, laying the foundation for meta-analysis.

MiR-21 Regulates TNF-α-Induced CD40 Expression via the SIRT1-NF-κB Pathway in Renal Inner Medullary Collecting Duct Cells.

BACKGROUND/AIMS: Recent studies have indicated that microRNA-21 (miR-21) is involved in the inflammatory response in relation to renal disease. Sirtuin1 (SIRT1) exerts renoprotective properties by counteracting inflammation. The activation of CD40 triggers inflammation that participates in renal inflammation and injury. The relationship between miR-21, SIRT1 and CD40, however, remains elusive. METHODS: Immunohistochemistry, small-interfering RNA (siRNA) transfection, quantitative real-time PCR and western blotting were applied to assess the morphological, functional and molecular mechanisms in primary cultured renal inner medullary collecting duct (IMCD) cells. RESULTS: TNF-α induced miR-21, CD40 and acetylated-NF-κBp65 (Ac-p65) expressions and reduced SIRT1 expression in IMCD cells. miR-21 mimics increased SIRT1 expression and attenuated Ac-p65 and CD40 expressions in TNF-α-induced IMCD cells, and the corresponding changes were observed with a miR-21 inhibitor. SIRT1 overexpression or activation by SRT1720 diminished TNF-α-induced CD40 and Ac-p65 expressions, which was reversed by SIRT1 siRNA or the inhibitors Ex527 and sirtinol and augmented by pretreatment with NF-κB siRNA. Further study found that the inhibitory effect of miR-21 on Ac-p65 and CD40 expressions was impeded by pretreatment with SIRT1 siRNA. CONCLUSION: The present study indicates that miR-21 inhibits TNF-α-induced CD40 expression in IMCD cells via the SIRT1-NF-κB signalling pathway, which provides new insight in understanding the anti-inflammatory effect of miR-21.

[Effect of aerobic interval training on the expression of renal CD40 in a rat model with myocardial infarction and its mechanism].

OBJECTIVE: To study the effects of aerobic interval training (AIT) on renal cluster of differentiation 40 (CD40) expression in rats with myocardial infarction (MI) and its possible mechanism. METHODS: Thirty-six rats were randomly divided into three groups (n=12):Sham, MI and MI with AIT (ME) groups. The MI model was established by ligation of the left anterior descending coronary artery. Treadmill training was performed five times a week for 8 weeks (AIT:60 min/day with 10 min of warm-up at 10 m/min and 50 min of exercise at 25 m/min 7 min interspersed with 3 min at 15 m/min). After training, cardiaorenal function and renal tissue remodeling were evaluated. The changes of CD40, high-sensitivity C reactive protein(hs-CRP), TNF-α, IL-6, p-NF-κBp65, blood urea nitrogen (BUN) and serum creatinine (sCr) were determined. RESULTS: Compared with the sham group, MI significantly increased left ventricular end-diastolic pressure (LVEDP) and decreased left ventricular systolic pressure (LVSP) and left indoor pressure change rate peak (dp/dtmax) in the MI group, concomitant with the increase in renal collagen volume fraction (CVF), which was reversed by AIT in the ME group. Moreover, compared with the sham group, CD40 was largely dispersed within the cytoplasm of renal tubule cells in the MI group. Meanwhile, the expressions of renal CD40 mRNA and protein, the levels of serum and renal hs-CRP, TNF-α and IL-6, the phosphorylation of NF-κBp65 (p-NF-κBp65) and the levels of sCr and BUN were obviously increased in the MI group. Compared with the MI group, AIT decreased the expressions of renal CD40 mRNA and protein, the levels of serum and renal hs-CRP, TNF-α and IL-6 and the expression of p-NF-κBp65, as well as decreased the levels of sCr and BUN in the ME group. CONCLUSIONS: AIT reduces the expressions of renal CD40 protein and mRNA, inhibits NF-κB signaling pathway, and then decreases the levels of inflammatory factors thereby improve the renal dysfunction after MI.

SIRT1 regulates lipopolysaccharide-induced CD40 expression in renal medullary collecting duct cells by suppressing the TLR4-NF-κB signaling pathway.

AIMS: Recent evidence indicates that sirtuin1 (SIRT1), an NAD+-dependent deacetylase, exerts a protective effect against inflammatory kidney injury by suppressing pro-inflammatory cytokines production. The co-stimulatory molecule, CD40, is expressed in a variety of inflammatory diseases in the kidney. Here, we aimed to investigate the potential effect of SIRT1 on CD40 expression induced by lipopolysaccharide (LPS) and to disclose the underlying mechanisms in renal inner medullary collecting duct (IMCD) cells. MAIN METHODS: mRNA and protein expressions were identified by quantitative real-time PCR and Western blot respectively. Subcellular localization of SIRT1 and CD40 were respectively detected by immunofluorescence and immunohistochemical staining. Small-interfering RNA (siRNA) was carried out for mechanism study. KEY FINDINGS: LPS reduced SIRT1 expression and up-regulated the expression of CD40, Toll-like receptor 4 (TLR4) and phospho-NF-κBp65 (p-NF-κBp65) in time- and concentration-dependent manners. Moreover, SIRT1 overexpression or activation by SRT1720 diminished the expression of CD40, TLR4 and p-NF-κBp65, which was reversed by SIRT1 siRNA or inhibitors Ex527 and sirtinol in LPS-stimulated IMCD cells. In addition, knockdown of TLR4 decreased the expression of CD40 and p-NF-κBp65 in IMCD cells exposed to LPS. Knockdown of NF-κBp65 or NF-κBp65 inhibition by pyrrolidine dithiocarbamate (PDTC) reduced LPS-induced CD40 expression in IMCD cells. Importantly, the inhibitory effect of SIRT1 on the expression of CD40 and p-NF-κBp65 was augmented by pre-treating with TLR4 siRNA. SIGNIFICANCE: Our data indicate that SIRT1 inhibits LPS-induced CD40 expression in IMCD cells by suppressing the TLR4-NF-κB signaling pathway, which might provide novel insight into understanding the protective effect of SIRT1 in kidney.

Sirtuin1 (SIRT1) Regulates Tumor Necrosis Factor-alpha (TNF-α-Induced) Aquaporin-2 (AQP2) Expression in Renal Medullary Collecting Duct Cells Through Inhibiting the NF-κB Pathway.

BACKGROUND Aquaporin-2 (AQP2) plays a major role in water reabsorption in the renal collecting duct, and is involved in a variety of renal disease. Recent studies have indicate that sirtuin1 (SIRT1) exerts renoprotective properties against kidney diseases. This study aimed to determine the potential role of SIRT1 in AQP2 expression induced by tumor necrosis factor-alpha (TNF-α) and to disclose the underlying mechanism in renal inner medullary collecting duct (IMCD) cells. MATERIAL AND METHODS Quantitative real-time PCR and Western blotting were respectively identified mRNA and protein expression. Immunofluorescence staining was used to detect the localization of AQP2. Small-interfering RNA (siRNA) was carried out for mechanism study. RESULTS Results showed that AQP2 was clearly increased in the plasma membrane and decreased in the cytoplasm of IMCD cells treated with AVP. TNF-α treatment in IMCD cells significantly reduced SIRT1 and AQP2 expression, and increased acetylated NF-κBp65 protein level in time- and concentration-dependent manners. Moreover, SIRT1 overexpression or the activator SRT1720 augmented AQP2 expression and reduced the acetylation of NF-κBp65, which was reversed by SIRT1 siRNA or the inhibitors Ex527 and sirtinol in TNF-α-induced IMCD cells. Knockdown of NF-κBp65 or NF-κBp65 inhibition by pyrrolidine dithiocarbamate (PDTC) enhanced AQP2 expression in IMCD cells exposed to TNF-α. Importantly, knockdown of NF-kBp65 augmented the up-regulation of SIRT1 on AQP2 expression in IMCD cells induced by TNF-α. CONCLUSIONS These findings indicate that SIRT1 increases AQP2 expression in TNF-α-induced IMCD cells via the NF-κB-dependent signalling pathway, which might provide novel insight to understanding the renoprotective effects of SIRT1 in kidney diseases.

Exercise training activates neuregulin 1/ErbB signaling and promotes cardiac repair in a rat myocardial infarction model.

AIMS: Exercise training (ET) has a cardioprotective effect and can alter the molecular response to myocardial infarction (MI). The Neuregulin 1 (NRG1)/ErbB signaling plays a critical role in cardiac repair and regeneration in the failing heart. We sought to investigate whether ET following MI could activate the NRG1/ErbB signaling and promote cardiac repair and regeneration. MAIN METHODS: Male Sprague-Dawley rats were used to establish the MI model. Exercise-trained animals were subjected to four weeks of exercise (16m/min, 50min/d, 5d/wk) following the surgery. AG1478 was used as an inhibitor of ErbB (1mg/kg body weight, administered i.v. every other day during the process of training). NRG1/ErbB signaling activation, cardiomyocyte (CM) proliferation and apoptosis were evaluated. KEY FINDINGS: In the exercise-trained rats, NRG1 expression was up-regulated and ErbB/PI3K/Akt signaling was activated compared with the MI group. In addition, ET preserved heart function accompanied with increased numbers of BrdU(+) CMs, PCNA(+) CMs and c-kit(+) cells, and reduced apoptosis level in the MI rats. In contrast, blocking ErbB signaling by AG1478 attenuated the ET-induced cardiac repair and regeneration. SIGNIFICANCE: ET up-regulates NRG1 expression and activates ErbB2, ErbB4 and PI3K/Akt signal transduction to promote cardiac repair through endogenous regeneration. Activation of ErbB may be an underlying mechanism for the ET-induced cardiac repair and regeneration following MI.

PPARα agonist fenofibrate attenuates TNF-α-induced CD40 expression in 3T3-L1 adipocytes via the SIRT1-dependent signaling pathway.

The ligand-activated transcription factor peroxisome proliferator-activated receptor-α (PPARα) participates in the regulation of cellular inflammation. More recent studies indicated that sirtuin1 (SIRT1), a NAD(+)-dependent deacetylase, regulates the inflammatory response in adipocytes. However, whether the role of PPARα in inflammation is mediated by SIRT1 remains unclear. In this study, we aimed to determine the effect of PPARα agonist fenofibrate on the expressions of SIRT1 and pro-inflammatory cytokine CD40 and underlying mechanisms in 3T3-L1 adipocytes. We found that fenofibrate inhibited CD40 expression and up-regulated SIRT1 expression in tumor necrosis factor-α (TNF-α)-stimulated adipocytes, and these effects of fenofibrate were reversed by PPARα antagonist GW6471. Moreover, SIRT1 inhibitors sirtinol/nicotinamide (NAM) or knockdown of SIRT1 could attenuate the effect of fenofibrate on TNF-α-induced CD40 expression in adipocytes. Importantly, NF-κB inhibitor pyrrolidine dithiocarbamate (PDTC) augmented the effect of fenofibrate on CD40 expression in adipocytes. Further study found that fenofibrate decreased the expression of acetylated-NF-κB p65 (Ac-NF-κB p65) in TNF-α-stimulated adipocytes, and the effect of fenofibrate was abolished by SIRT1 inhibition. In addition, fenofibrate up-regulated SIRT1 expression through AMPK in TNF-α-stimulated adipocytes. Taken together, these findings indicate that PPARα agonist fenofibrate inhibits TNF-α-induced CD40 expression in 3T3-L1 adipocytes via the SIRT1-dependent signaling pathway.

SIRT1 inhibits TNF-α-induced apoptosis of vascular adventitial fibroblasts partly through the deacetylation of FoxO1.

Sirtuin 1 (SIRT1), a NAD(+)-dependent class III histone deacetylase, participates in regulating cellular apoptosis, senescence and metabolism by deacetylating histones and multiple transcription factors. In this study, we aimed to determine the effect of SIRT1 on the apoptosis of vascular adventitial fibroblasts (VAFs) and related signaling pathways. SIRT1 was found in the nucleus of VAFs and translocated into the cytoplasm in response to tumor necrosis factor-α (TNF-α). Moreover, SIRT1 protein expression was reduced in VAFs stimulated with TNF-α. In addition, TNF-α increased the apoptosis of VAFs. Activation of SIRT1 by resveratrol (RSV) or overexpression of SIRT1 attenuated TNF-α-induced VAF apoptosis by decreasing the percentage of apoptotic cells and cleaved caspase-3 protein expression and increasing the Bcl-2/Bax ratio. In contrast, inhibition of SIRT1 by sirtinol/nicotinamide or knockdown of SIRT1 enhanced apoptosis of VAFs. On the other hand, knockdown of FoxO1 reduced TNF-α-induced VAF apoptosis. SIRT1 interacted with FoxO1 in VAFs by the co-immunoprecipitation assay. Further study showed that RSV or SIRT1 overexpression decreased acetylated-FoxO1 (Ac-FoxO1) protein expression in VAFs stimulated with TNF-α. Knockdown of SIRT1 resulted in an increase in Ac-FoxO1 protein expression. Taken together, these findings indicate that SIRT1 inhibits the apoptosis of VAFs, whereas FoxO1 promotes VAF apoptosis. Furthermore, the inhibitory effect of SIRT1 on VAF apoptosis is partly mediated by the deacetylation of FoxO1.

SIRT1 regulates CD40 expression induced by TNF-α via NF-ĸB pathway in endothelial cells.

BACKGROUND: Compelling evidence suggests that SIRT1, NAD(+)-dependent class III protein deacetylase, plays an important role in the prevention and treatment of atherosclerosis by counteracting inflammation. Cluster of differentiation 40 (CD40), as a pro-inflammatory cytokine, has been shown to participate in the pathophysiology of atherosclerosis. The relationship between SIRT1 and CD40, however, remained elusive. The present study was thus designed to explore the potential effect of SIRT1 on CD40 expression induced by tumor necrosis factor-α (TNF-α) and to disclose the underlying mechanism in CRL-1730 endothelial cells. METHODS: mRNA and protein expressions were identified by quantitative real-time PCR and Western blot respectively. Subcellular localization of SIRT1 was detected by immunofluorescence analysis. SIRT1 small-interfering RNA (siRNA) was carried out for mechanism study. RESULTS: TNF-α reduced SIRT1 expression and induced CD40 expression in CRL-1730 endothelial cells in a time- and concentration- dependent manner. Pretreatment with resveratrol (a potent SIRT1 activator) inhibited TNF-α-induced CD40 expression, while pretreatment with nicotinamide (class b HDACs inhibitor nicotinamide) or sirtinol (a known SIRT1 inhibitor), especially SIRT1 siRNA significantly augmented TNF-α-induced CD40 expression. The frther sudy idicated that PDTC (NF-ĸB inhibitor) pretreatment attenuated TNF-α-induced CD40 expression, and SIRT1 siRNA significantly augmented TNF-α-induced acetylated-NF-ĸB p65 (Lys310) expression. CONCLUSION: The present study provides the direct evidence that SIRT1 can inhibit TNF-α- induced CD40 expression in CRL-1730 endothelial cells by deacetylating the RelA/p65 subunit of NF-ĸB at lysine 310, which provides new insights into understanding of the anti-inflammatory and anti-athroscerotic actions of SIRT1.

SIRT1 regulates TNF-α-induced expression of CD40 in 3T3-L1 adipocytes via NF-κB pathway.

Sirtuin1 (SIRT1), a NAD(+)-dependent deacetylase, not only regulates lipid and glucose homeostasis, but also involves the regulation of proinflammatory cytokine involved in inflammation-associated diseases. The activation of CD40 triggers inflammation that plays a crucial role in the development of many chronic inflammatory diseases including obesity. Growing evidence indicated that SIRT1 exerts anti-inflammatory properties by suppressing proinflammatory cytokines production. However, the effect of SIRT1 on the expression of CD40 in adipocytes has not yet been fully elucidated. The present study showed that SIRT1 expressed both in the nucleus and cytoplasm of 3T3-L1 adipocytes. TNF-α significantly reduced the expression of SIRT1 mRNA and protein and increased the expression of CD40 mRNA and protein in time- and concentration-dependent manners. Overexpression of SIRT1 or SIRT1 activation by resveratrol obviously attenuated the expression of CD40 induced by TNF-α in 3T3-L1 adipocytes, whereas knockdown of SIRT1 or SIRT1 inhibition by nicotinamide and sirtinol significantly enhanced TNF-α-induced expression of CD40. Furthermore, overexpression of SIRT1 or SIRT1 activation by resveratrol diminished TNF-α-induced acetylation of NF-κBp65, while knockdown of SIRT1 or SIRT1 inhibition by nicotinamide and sirtinol augmented TNF-α-induced acetylation of NF-κBp65 in 3T3-L1 adipocytes. NF-κB inhibitor PDTC reduced TNF-α-induced mRNA and protein expression of CD40 in 3T3-L1 adipocytes. The combination treatment of resveratrol and PDTC significantly reduced TNF-α-induced expression of CD40, and the inhibitory effects were higher than that of the single treatment. Taken together, SIRT1 exerts anti-inflammatory property by regulating TNF-α-induced expression of CD40 partially through the NF-κB pathway in 3T3-L1 adipocytes. More importantly, the regulation of SIRT1 on the expression of CD40 provides new insight to understand the anti-inflammatory effects of SIRT1.

Protective effects of paeoniflorin against cobalt chloride-induced apoptosis of endothelial cells via HIF-1α pathway.

Accumulating evidence has suggested the importance of hypoxia in the initiation and development of atherosclerotic lesion, and hypoxia has a profound impact on endothelial cell properties during cardiovascular disease processes. Paeoniflorin, isolated from the root of Paeonia lactiflora pall, can protect endothelial cells from hypoxic damage in a variety of ways, such as by enhancing the production of nitric oxide (NO) and decreasing the expressions of intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1). This study evaluated the protective effects of paeoniflorin against cobalt chloride (CoCl2, a hypoxia-mimicking agent)-induced apoptosis of endothelial cells (CRL-1730) and the underlying mechanisms in vitro. Endothelial cells were exposed to CoCl2 with or without pre-treatment with different concentrations of paeoniflorin. After treated with 0.6mM CoCl2 for 24 h, endothelial cells showed significant decrease in cell viability and increased apoptosis rate, which could be reversed by pre-treatment with paeoniflorin. Similarly, pre-treatment with paeoniflorin could prevent CoCl2-induced hypoxia-induced factor-1α (HIF-1α) accumulation and down-regulate the expressions of p53 and Bcl-2/adenovirus E1B 19kDa interacting protein 3 (BNIP3). These findings indicate that paeoniflorin had effective protection against hypoxia-induced apoptosis of endothelial cells and that HIF-1α, p53 and BNIP3 might be involved in this process.

The roles of buyang huanwu decoction in anti-inflammation, antioxidation and regulation of lipid metabolism in rats with myocardial ischemia.

Buyang Huanwu Decoction (BYHWD) is a well-known Chinese medicine formula. Recent studies have reported that BYHWD can be used to treat ischemic heart disease. This study investigated the potential mechanism underlying the roles of BYHWD in alleviating the myocardial ischemia induced by isoproterenol (ISO) in rats. Different doses of BYHWD (25.68, 12.84 and 6.42 g kg(-1)) were lavaged to rats, respectively. Then the expression of the cluster of differentiation 40 (CD40) in the mononuclear cells was measured using flow cytometry, and the expressions of CD40 and its ligand (CD40L) in myocardial tissues were determined by western blotting. The serum biochemical values of superoxide dismutase (SOD) activity, the malondialdehyde (MDA) level and the free fatty acid (FFA) content were measured. The results showed that the SOD activities of BYHWD groups were significantly higher than that of the ISO group, while the MDA levels and FFA contents of all BYHWD groups were lower than that of the ISO group. BYHWD could decrease the expression of CD40 in the mononuclear cells and the CD40 and CD40L expressions in myocardial tissues. Our data suggest that the roles of BYHWD are not only related to its antioxidative action and regulation of lipid metabolisms, but also to the inhibition of inflammatory pathway by the decreased CD40 and CD40L expressions in rats with myocardial ischemia.

The effects of Buyang Huanwu Decoction on hemorheological disorders and energy metabolism in rats with coronary heart disease.

ETHNOPHARMACOLOGICAL RELEVANCE: Buyang Huanwu Decoction (BYHWD), a traditional Chinese medicine (TCM) formula, has been recognized as a clinical treatment for coronary heart disease (CHD) with qi deficiency and blood stasis syndrome. The effects of BYHWD on hemorheological disorders and energy metabolism in CHD with qi deficiency and blood stasis syndrome are still unclear. AIM OF THE STUDY: To investigate whether the ameliorative effects of BYHWD on CHD rats with qi deficiency and blood stasis syndrome are associated with the regulation of hemorheological disorders and energy metabolism. MATERIALS AND METHODS: The rats were lavaged with 25.68, 12.84 and 6.42 g/kg BYHWD (g weight of mixed crude drugs/kg body weight), respectively, once a day for 21 days. The body weight, exhaustive swimming time and tongue characters were observed and recorded. The whole blood viscosity and plasma viscosity were determined by hematology analyzer. The level of fibrinogen (Fbg) in plasma was determined by using Fbg assay kit. The platelet aggregation induced by adenosine diphosphatase was measured by semi-automatic whole blood platelet analyzer. The level of blood glucose (BG) was determined by LifeScan. The activity of Na(+)-K(+)-ATPase in heart tissues was detected by spectrophotometer. RESULTS: BYHWD improved the exterior signs of qi deficiency and blood stasis syndrome in rats with CHD, including the body weight, exhaustive swimming time and tongue quality. The whole blood viscosity in rats treated with 25.68 g/kg BYHWD decreased at the shear rate of 10s(-1) (P<0.05) and the plasma viscosity decreased in rats treated with 25.68 and 12.84 g/kg BYHWD (P<0.05). The plasma Fbg level and the platelet aggregation decreased in rats treated with 25.68 g/kg BYHWD (P<0.01). The results also revealed that the BG level decreased and the Na(+)-K(+)-ATPase activity in heart tissues increased in rats treated with 25.68 and 12.84 g/kg BYHWD (P<0.01). CONCLUSION: The results suggest that the ameliorative effects of BYHWD on CHD rats with qi deficiency and blood stasis syndrome are mediated by the improvement of hemorheological disorders and energy metabolism.

Effect of exercise training on renal function and renal aquaporin-2 expression in rats with chronic heart failure.

1. Chronic heart failure (CHF) is often accompanied by renal dysfunction. Exercise training may relieve the symptomatic burden and improve the overall prognosis of CHF. In the present study, the effects of exercise training on renal function and renal aquaporin (AQP)-2 expression in CHF rats were examined to determine whether exercise training could relieve renal dysfunction in CHF rats. 2. Male Sprague-Dawley rats were divided into three groups: sham, sedentary CHF (Sed-CHF) and exercise training CHF (Ex-CHF) groups. Cardiorenal function was assessed in each group by haemodynamic measurement and ultraviolet spectrophotometry. Pathological changes in cardiac and renal tissues were evaluated histologically and the collagen volume fraction (CVF) was calculated. The expressions of AQP-2 and ß-tubulin were determined by western blotting and immunohistochemistry. 3. The Sed-CHF rats were found to have increased left ventricular end-diastolic pressure (LVEDP) and CVF in the heart compared with sham rats. Exercise training decreased LVEDP and CVF values in Ex-CHF rats. The Sed-CHF rats were found to have increased serum levels of creatinine (sCr), blood urea nitrogen (BUN) and arginine vasopressin (AVP), as well as increased CVF in the kidney, compared with sham rats. Exercise training decreased levels of sCr, BUN, AVP and CVF in Ex-CHF rats. Moreover, exercise training decreased AQP-2 and ß-tubulin protein expression in the kidney of CHF rats. 4. The results suggest that exercise training can significantly improve the renal dysfunction in CHF rats and that the underlying mechanism may be related to water reabsorption and preventing changes to the cytoskeleton.

Protective effects of chinese traditional medicine buyang huanwu decoction on myocardial injury.

Many clinical studies have reported that Buyang Huanwu Decoction (BYHWD) has a protective effect on ischemic heart disease (IHD). In the present study, the protective effect of BYHWD on myocardial ischemia was investigated. Different doses of BYHWD and Compound Danshen Dropping Pills (CDDP) were lavaged to rats, respectively, isoproterenol (ISO) was intraperitoneally injected in to all animals to induce myocardial ischemia except the control group. Electrocardiogram (ECG) of each animal was recorded; activities of lactate dehydrogenase (LDH), creatine kinase (CK) and aspartate aminotransferase (AST) in serum were detected. As the results of ECG showed, pre-treatment with BYHWD inhibited ischemic myocardial injury, and the activities of LDH, CK and AST were lower than those in the myocardial ischemia model group, which suggests that BYHWD rescues the myocardium from ischemia status. To research the potential mechanism, the level of nitric oxide (NO), nitric oxide syntheses (NOS) and inducible nitric oxide syntheses (iNOS), the expression of iNOS and ligand of cluster of differentiation 40 (CD40L) were detected. The results revealed that BYHWD significantly decreased the level of NO, NOS and iNOS in serum. Moreover, BYHWD decreased the expression of iNOS and CD40L in myocardial tissues. These results indicate that the protective effect of BYHWD on myocardial ischemia and mechanism are associated with inhibition of iNOS and CD40L expression.