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This review addresses the issues of low consumer engagement and market development difficulties in intangible cultural heritage (ICH) products. Dietary ICH products are selected as research materials to discover contemporary commercial survival paths for ICH through the psychological effects of advertising. Firstly, this study examines the respective advantages of rational and emotional ICH advertisement in terms of emotional responses, cognitive responses, attitudes, recall, and recognition. Then, it explores the effects of different ICH advertisement types (rational advertisement, emotional advertisement) and different degrees of situational involvement (purchasing for oneself, purchasing gifts for others) on the advertising effectiveness, aiming to identify factors influencing the psychological effects of ICH advertisement. Through statistical analysis, the main conclusions are as follows: (1) Rational ICH advertisement prompts consumers to consider the actual attributes of ICH products, leading to a more positive purchasing attitude. (2) Emotional ICH advertisement is more effective in eliciting positive emotions from consumers and enhancing brand memory. (3) Under the scenario of purchasing a gift for others, emotional ICH advertisement has a more positive impact on consumers' attitudes towards advertising. (4) Under different degrees of situational involvement, rational ICH advertisement has a more positive impact on consumers' purchasing attitudes. This study not only provides guidance for optimizing ICH advertising strategies but also offers new directions for market expansion, contributing valuable insights into cultural heritage preservation, as well as the development and protection of ICH. [ABSTRACT FROM AUTHOR]

This paper describes the introduction of an open-access preprint server in China covering 43 disciplines. The system includes mandatory deposit for state-funded research and reports on the repository and its effectiveness and outlines a novel process of peer-review of preprints in the repository, which can be incorporated into the established system of promotion and tenure. This state-initiated innovation is considered to have been well incorporated into the established scientific communication system despite the sociological differences between the various disciplines served by the repository. (Contains 3 figures and 2 tables.)

Atherosclerotic cardiovascular disease is a major cause of morbidity and mortality in the Western world. Despite tremendous strides in understandings its pathogenesis, it still remains a challenge because of gaps in our understanding of its initiation, progression and complications leading to the clinical syndromes of angina, acute coronary syndrome, cerebrovascular disease and peripheral vascular disease. Recent studies have provided impetus on the shift from models of atherosclerosis based on cellular interactions to models where the important role of extracellular matrix is recognized. Proteoglycans, especially those belonging to the small leucine-rich proteoglycan family of which decorin is a representative example, have come under close scrutiny for their role in atherogenesis. There is evidence from in vitro and in vivo animal models as well as humans to suggest an important role of decorin in attenuating progression of atherosclerosis. Decorin distribution in different blood vessels has been shown to inversely correlate with the tendency to develop atherosclerosis. Decorin seems to interact closely with different cellular components of the plaque milieu, thereby suggesting its role in influencing atherogenesis at different steps. Here we review the current understanding of the role of decorin in the pathogenesis of atherosclerosis. [ABSTRACT FROM PUBLISHER]

Abstract: Seizure is one kind of severe side effects during clozapine (Clo) treatment. However, the mechanism of seizure associated with Clo therapy is not completely clear. Strychnine-sensitive glycine receptors (GlyRs) play an important role in regulating the excitability in the hippocampus. In the present study, we investigated the effect of Clo on GlyRs in cultured hippocampal neurons of rats. Clo reversibly inhibited the glycine-induced chloride currents (I Gly) in a concentration-dependent manner. The half-maximal effect concentration (EC50) for glycine alone was 25.6±0.7 μM with the Hill coefficient 1.5±0.1; in the presence of Clo, the EC50 and the Hill coefficient were 28.9±6.3 μM and 1.2±0.3 respectively, which were not significantly affected by Clo. In addition, Clo inhibition of I Gly was not influenced by blocking D1 and D2 dopamine receptors with haloperidol (Hal). Taken together, these results suggest that Clo is a non-competitive antagonist of GlyR independent of its activation of dopamine receptors, which may contribute to seizure associated with Clo therapy. [Copyright &y& Elsevier]

Abstract: LOX-1, a cell surface lectin-like receptor, is upregulated by oxidized low-density lipoprotein (ox-LDL) and angiotensin II (Ang II), and plays an important role in host defense. The specific C-type lectin domain on LOX-1 is essential for ox-LDL binding and internalization, generation of oxidant species and eliciting immune response. Here, we show that LOX-1 deletion alters genes that relate to immune response. Microarray (and qPCR) analysis of cardiac tissues showed downregulated expression of several immunoglobulins (Igk-V8, Igk-C, Igh-6, Igj, Ighg, Igh, and Igl-V1) in the LOX-1 knockout (KO) mice [p <0.05 vs. the wild-type (WT) mice]. The expression of these immunoglobulins was upregulated several-fold in the LOX-1 KO mice hearts when these mice were infused with Ang II (p <0.05, vs. WT mice). Importantly, cultured mouse HL-1 cardiomyocytes expressed these immunoglobulins, and pretreatment of cardiomyocytes with a specific anti-LOX-1 antibody enhanced the generation of immunoglobulins upon subsequent exposure to Ang II. These observations mirrored the data obtained from WT and LOX-1 KO mice hearts in the resting state and following Ang II infusion. This study provides first set of data on immunoglobulin expression in cardiac tissues of WT and LOX-1 KO mice and in cultured HL-1 cardiomyocytes, and demonstrates that LOX-1 inactivation leads to upregulation of immunoglobulins in cardiomyocytes upon challenge with Ang II. [Copyright &y& Elsevier]

Abstract: Atherogenesis is associated with inflammation and oxidative stress. Activation of renin-angiotensin system with generation of angiotensin II and type 1 receptor (AT1R) stimulation has been amply reported in atherosclerosis. Since angiotensin II type 2 receptor (AT2R) activity is purported to oppose the effects of AT1R, we hypothesized that AT2R (agtr2) over-expression would inhibit atherogenesis. We prepared recombinant adeno-associated virus type-2 (AAV) carrying AT2R cDNA (AAV/AT2R), and homozygous LDLR-deficient (KO) mice were given AAV/AT2R, AAV/Neo or saline. All mice were placed on a high cholesterol diet. After 18 weeks, AT2R was found to be over-expressed systemically in AAV/AT2R-treated mice. Atherogenesis in aorta was reduced in the AAV/AT2R group by ≈50% compared to other LDLR KO mice groups. Expression of NADPH oxidase, nitrotyrosine and NF-κB was increased in aortic tissues of the LDLR KO mice given saline or AAV/Neo, but not in mice with AT2R upregulation. Expression of endothelial nitric oxide synthase (eNOS) and heme-oxygenase-1 (HO-1) was decreased and that of the lectin-like oxidized-LDL receptor (LOX-1) increased in the LDLR KO mice, but not in the mice with AT2R over-expression. Further, Akt-1 phosphorylation was reduced in the LDLR KO mice, but not in the mice with AT2R over-expression. Thus, AT2R upregulation can reduce atherogenesis, possibly by modulating oxidative stress and the pro-inflammatory cascade, mediated via Akt-1. Over-expression of AT2R may be an important therapeutic approach in atherosclerosis. [Copyright &y& Elsevier]

Abstract: LOX-1 is a newly described lectin-like receptor for oxidized-LDL (ox-LDL), which is over-expressed in the ischemic myocardium. To examine the pathogenic role of LOX-1 in the determination of ischemia–reperfusion (I–R) injury to the heart, we developed LOX-1 knockout (KO) mice, and subjected these mice to 60 min of left coronary artery occlusion followed by 60 min of reperfusion. I–R in the LOX-1 KO mice resulted in a significant reduction in myocardial injury as well as in accumulation of inflammatory cells in the I–R myocardium and lipid peroxidation (P <0.01 vs. wild-type mice). Concomitantly, there was significant preservation of cardiac function in the LOX-1 KO mice despite I–R (P <0.01 vs. the wild-type mice). The phosphorylation of oxidative stress-sensitive mitogen-activated protein kinase (p38MAPK) and protein kinase B/Akt-1, expression of nitrotyrosine and inducible nitric oxide synthase (iNOS), and superoxide dismutase activity were enhanced during I–R in the wild-type mice. These alterations in p38MAPK, Akt-1 and iNOS were much less pronounced in the LOX-1 KO mice. The superoxide dismutase activity increased further in the LOX-1 KO mice. These observations provide compelling evidence that LOX-1 may be a key modulator of myocardial I–R injury, and its effect is mediated by pro-oxidant signals. LOX-1 may be a potential target for therapy of myocardial ischemic injury. [Copyright &y& Elsevier]

Abstract: Objective: Chronic ischemia is associated with alterations in genes that result in myocardial remodeling. An important biochemical basis of cardiac remodeling is generation of reactive oxygen species (ROS). A few studies have suggested that acute ischemia triggers signals for remodeling. We examined the hypothesis that targeted deletion of lectin-like oxidized-LDL receptor (LOX-1) may inhibit signals related to cardiac remodeling. Methods and results: We generated LOX-1 knockout (KO) mice on C57BL/6 (wild-type mice) background, and subjected wild-type and KO mice to ischemia–reperfusion (I–R). The wild-type mice developed a marked reduction in left ventricular systolic pressure and ±dp/dtmax and an increase in left ventricular end-diastolic pressure following I–R, and this change was much less in the LOX-1 KO mice, indicating preservation of left ventricular function with LOX-1 deletion. There was evidence for marked oxidative stress (NADPH oxidase expression, malondialdehyde and 8-isoprostane) following I–R in the wild-type mice, much less so in the LOX-1 KO mice (P <0.01). In concert, collagen deposition (Masson''s trichrome and Picro-sirius red staining) increased dramatically in the wild-type mice, but only half as much in the LOX-1 KO mice (P <0.01). Collagen staining data was corroborated with procollagen-I expression. Further, fibronectin and osteopontin expression increased in the wild-type mice, but to a much smaller extent in the LOX-1 KO mice (P <0.01). Conclusions: These findings provide compelling evidence that LOX-1 is a key modulator of cardiac remodeling which starts immediately following I–R. [Copyright &y& Elsevier]

Highlights: [•] Most of macrophage accumulation in atherosclerotic tissues is on the adventitial and subendothelial regions of the artery. [•] Macrophage accumulation increases until 12weeks of high cholesterol feeding to mice and then begins to decline. [•] LOX-1 deletion reduces macrophage accumulation by reducing migration potential of these cells. [Copyright &y& Elsevier]

Mulberry leaf, an important traditional Chinese medicine, possesses many biological activities, including effects of anti-obesity. However, which constituents of mulberry leaf are responsible for its anti-adipogenic action is unclear. This study primarily investigated the chemical constituents from mulberry leaf and their bioactivity on the proliferation and differentiation of 3T3-L1 preadipocytes. A new flavane derivative, (2 S )-4′-hydroxy-7-methoxy-8-prenylflavan ( 1 ), together with twelve known compounds including three flavanes ( 2 – 4 ), three chalcones ( 5 – 7 ), two flavones ( 8 – 9 ), two benzofurans ( 10 – 11 ) and two coumarin ( 12 – 13 ) was isolated from mulberry leaf. The structure of the new compound was elucidated by various spectroscopic methods including UV, HR-ESI-MS, 1 H and 13 C NMR and CD. The results of activity screening showed that compound 2 , 6 and 7 inhibited the proliferation and differentiation of 3T3-L1 preadipocytes. [ABSTRACT FROM AUTHOR]

Highlights: [•] VPO1 was over-expressed in hypertensive SHRs as compared to WKY rats. [•] VPO1 over-expression was accompanied by increased oxidative stress. [•] VPO1 over-expression was found to be related to impaired endothelial function. [ABSTRACT FROM AUTHOR]

It is assumed that acute myocardial infarction affects renal function. To study the mechanism, we used mice following permanent ligation of their left coronary artery that results in extensive myocardial infarction. Soon after ligation, there was a marked rise in circulating pro-inflammatory cytokines and malondialdehyde (thiobarbituric acid-positive evidence of lipid peroxidation). Renal function had significantly declined by the third day in association with mild fibrosis, and swelling of glomeruli and tubules. There was a significant increase in the expression of the lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1), interelukin-1β, vascular cell adhesion molecule-1, and thiobarbituric acid-reactive substances in the kidney. Renal function showed some recovery by Day 21; however, there was progressive fibrosis of the kidneys. LOX-1 knockout mice had significantly diminished increases in systemic and renal pro-inflammatory cytokines, malondialdehyde, structural alterations, and decline in renal function than the wild-type mice following ligation of the left coronary artery. Cardiac function and survival rates were also significantly better in the LOX-1 knockout mice than in the wild-type mice. Hence, severe myocardial ischemia results in renal dysfunction and histological abnormalities suggestive of acute renal injury. Thus, LOX-1 is a key modulator among multiple mechanisms underlying renal dysfunction following extensive myocardial infarction. [ABSTRACT FROM AUTHOR]

Abstract: Previous studies have indicated that GABAergic disinhibition contributes to cognitive deficits mediated by NMDA receptor hypofunction in schizophrenia model of rats. However, the underlying mechanism of GABAergic disinhibition in schizophrenia remains elusive. In this study, we found that the maintenance of long term potentiation (LTP) was impaired in the hippocampus of rats with MK-801-induced cognitive impairments. The impairment of LTP maintenance was significantly reversed by picrotoxinin, a specific GABAA receptor-chloride channel blocker and furosemide, a K+–Cl− cotransporter 2 (KCC2) blocker, respectively. Furthermore, immunoblotting results indicated KCC2 expression in hippocampal CA1 of MK-801-treated rats was lower than that of normal rats before LTP induction. Additionally, LTP-accompanied downregulation of KCC2 was prevented in MK-801-treated rats during LTP induction. Our results suggested that KCC2 expression in hippocampal CA1 of MK-801-treated rats was not further decreased by LTP induction because of its low expression caused by MK-801 treatment. Accordingly, GABAergic inhibition was not further decreased during LTP induction due to the depressed basal GABAergic tone in MK-801-treated rats, Therefore, GABAergic disinhibition in MK-801-treated rats restricts the further downregulation of KCC2 during LTP induction and contributes to the stable GABAergic inhibition and the impaired LTP expression. Our results thus reveal the mechanism that GABAergic disinhibition contributes to cognitive deficits. [Copyright &y& Elsevier]

Continuous recruitment and inappropriate activation of platelets in pulmonary arteries contribute to pulmonary vascular remodeling in pulmonary hypertension (PH). Our previous study has demonstrated that lectin like oxidized low-density lipoprotein receptor-1 (LOX-1) regulates the proliferation of pulmonary arterial smooth muscle cells (PASMCs). Phosphatidylserine exposed on the surface of activated platelets is a ligand for LOX-1. However, whether hypoxia-activated platelets stimulate the proliferation and migration of PASMCs by phosphatidylserine/LOX-1 signaling-impelled intercellular communication remains unclear. The present study found that rats treated with hypoxia (10% O 2) for 21 days revealed PH with the activation of platelets and the recruitment of platelets in pulmonary arteries, and LOX-1 knockout inhibited hypoxia-induced PH and platelets activation. Notably, co-incubation of PASMCs with hypoxic PH rats-derived platelets up-regulated LOX-1 expression in PASMCs leading to the proliferation and migration of PASMCs, which was inhibited by the phosphatidylserine inhibitor annexin V or the LOX-1 neutralizing antibody. LOX-1 knockout led to decreased proliferation and migration of PASMCs stimulated by hypoxia-activated platelets. In rats, hypoxia up-regulated the phosphorylation of signal transducer and activator of transcription 3 (Stat3) and the expression of Pim-1 in pulmonary arteries. Hypoxia-activated platelets also up-regulated the phosphorylation of Stat3 and the expression of Pim-1 in PASMCs, which was inhibited by annexin V, the LOX-1 neutralizing antibody, the protein kinase C inhibitor and LOX-1 knockout. In conclusion, we for the first time demonstrated that hypoxia-activated platelets stimulated the proliferation and migration of PASMCs by phosphatidylserine/LOX-1/PKC/Stat3/Pim-1 signaling-impelled intercellular communication, thereby potentially contributing to hypoxic pulmonary vascular remodeling. • Continuous recruitment and inappropriate activation of platelets in PAs contribute to pulmonary vascular remodeling in PH. • Phosphatidylserine (PS) exposed on the surface of activated platelets is a ligand for LOX-1. • PS/LOX-1 signaling-impelled intercellular communication mediating the interaction between platelets and PASMCs is unclear. • Hypoxia-activated platelets stimulated the proliferation and migration of PASMCs by PS/LOX-1/PKC/Stat3/Pim-1signaling. [ABSTRACT FROM AUTHOR]

Phase shifting fringe projection profilometry is a widely used optical 3D surface measurement method due to its high resolution, high speed, and full-field inspection. However, the measurement accuracy decreases in regions with a reflectivity or distance discontinuity. To this end, first, a general continuous quasi-one-dimensional phase error model is proposed for discontinuity representation. Second, the discontinuities are further divided into degenerate and nondegenerate discontinuities to improve the computational speed. Third, a phase error compensation algorithm is proposed with a parameter estimation method to improve the measurement accuracy. Simulations and experiments demonstrate that the proposed methods are effective.

Background: Coronavirus disease 2019 (COVID-19) is highly contagious and deadly and is associated with coagulopathy. Pentraxin-3(PTX3) participates in innate resistance to infections and plays a role in thrombogenesis., Purpose: The present study aimed to investigate the role of PTX3 in coagulopathy in patients with COVID-19., Methods: A retrospective study, including thirty-nine COVID-19 patients, enrolled in Hunan, China, were performed. The patients were classified into the D-dimer&#95;L (D-dimer <1mg/L) and D-dimer&#95;H (D-dimer≥1mg/L) groups basing on the plasma D-dimer levels on admission. Serum PTX3 levels were detected by enzyme-linked immunosorbent assays and compared between those two groups, then receiver operating characteristic (ROC) curve analysis, correlation analysis, and linear regression models were performed to analyze the association between PTX3 and D-dimer., Results: Our results showed that serum PTX3 levels (median values, 10.21 vs. 3.36, P <0.001), computerized chest tomography (C.T.) scores (median values, 10.0 vs. 9.0, P <0.05), and length of stay (LOS) (mean values, 16.0 vs. 10.7, P =0.001) in the D-dimer&#95;H group were significantly higher than that in D-dimer&#95;L group. ROC curve analysis revealed that the AUC of white blood corpuscle counts, C-reaction protein, erythrocyte sedimentation rate, and PTX3 for COVID-19 were 0.685, 0.863, 0.846, and 0.985, respectively. Correlation analysis showed that there was a positive relationship between PTX3 and D-dimer (r=0.721, P <0.001), chest CT imaging score (r=0.418, P =0.008), and LOS (r=0.486, P =0.002). Multiple linear regression analysis showed that the coefficient of determination was 0.657 ( P < 0.001)., Conclusion: Serum level of PTX3 was positively correlated with disease severity and coagulopathy. Detection of serum PTX3 level could help identify severer patients on admission and may be a potential therapeutic target for coagulopathy in patients with COVID-19., Competing Interests: Competing interests: The authors declare no conflict of Interest.

Recent studies revealed that sirtuin 1 (SIRT1) is involved in the regulation of energy metabolism and its agonist resveratrol showed anti-obesity effect. This study aims to determine whether BTM-0512, a novel derivative of resveratrol, acts as an antagonist of obesity and to explore its possible mechanisms. High-fat diet (HFD)-induced obese mice were intragastrically administered with BTM-0512 (5, 10, and 20 mg/kg/day) or resveratrol (10 mg/kg/day). It was found that the body weight, Lee's index, ratio of visceral adipose tissue (VAT) to body weight, and blood glucose were significantly reduced in BTM-0512-treated mice when compared with those in mice treated with resveratrol. BTM-0512 up-regulated the expressions of SIRT1, full length PRDM16 (fPRDM16), total PRDM16 (tPRDM16, including fPPRDM16 and other PRDM16 isoforms), and uncoupling protein 1 (UCP1) in both brown and subcutaneous adipose tissues. Although BTM-0512 and resveratrol also up-regulated SIRT1 and tPRDM16 levels in VAT of HFD-induced obese mice, the expressions of fPRDM16, UCP1, and TMEM26 were down-regulated. In mouse primary subcutaneous preadipocytes cultured with or without adipogenic medium, BTM-0512 up-regulated fPRDM16, tPRDM16, and UCP1 expressions, which was reversed by SIRT1 antagonists. But in cultured brown and visceral adipocytes, the UCP1 protein level showed no significant change after treatment with 1 μM of BTM-0512. Moreover, transfection with human SIRT1 plasmid reduced lipid deposit, as well as the mRNA levels of fPRDM16, UCP1, and TMEM26, in cultured human visceral adipose-derived stem cells. In conclusion, BTM-0512 has stronger anti-obesity effect than resveratrol, which might be associated with activation of beige remodeling in subcutaneous adipose tissue., (© The Author 2017. Published by Oxford University Press on behalf of the Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.)

Objective: To explore the role of calpain in pulmonary vascular remodeling in hypoxia-induced pulmonary hypertension and the underlying mechanisms.
, Methods: Sprague-Dawley rats were randomly divided into the hypoxia group and the normoxia control group. Right ventricular systolic pressure (RVSP) and mean pulmonary artery pressure (mPAP) were monitored by a method with right external jugular vein cannula. Right ventricular hypertrophy index was presented as the ratio of right ventricular weight to left ventricular weight (left ventricle plus septum weight). Levels of calpain-1, -2 and -4 mRNA in pulmonary artery were determined by real-time PCR. Levels of calpain-1, -2 and -4 protein were determined by Western blot. Primary rat pulmonary arterial smooth muscle cells (PASMCs) were divided into 4 groups: a normoxia control group, a normoxia+MDL28170 group, a hypoxia group and a hypoxia+MDL28170 group. Cell proliferation was detected by MTS and flow cytometry. Levels of Ki-67 and proliferating cell nuclear antigen (PCNA) mRNA were determined by real-time PCR.
, Results: RVSP, mPAP and right ventricular remodeling index were significantly elevated in the hypoxia group compared to those in the normoxia group. In the hypoxia group, pulmonary vascular remodeling was significantly developed, accompanied by up-regulation of calpain-1, -2 and -4. MDL28170 significantly inhibited hypoxia-induced proliferation of PASMCs concomitant with the suppression of Ki-67 and PCNA mRNA expression.
, Conclusion: Calpain mediates vascular remodeling via promoting proliferation of PASMCs in hypoxia-induced pulmonary hypertension.

Aims: Oxidative stress and inflammation are leading risk factors for age-associated functional declines. We assessed aspirin effects on endogenous oxidative-stress levels, lifespan, and age-related functional declines, in the nematode Caenorhabditis elegans., Results: Both aspirin and its salicylate moiety, at nontoxic concentrations (0.5-1 mM), attenuated endogenous levels of reactive oxygen species (p<0.001), and upregulated antioxidant genes encoding superoxide dismutases (especially sod-3, p<0.001), catalases (especially ctl-2, p<0.0001), and two glutathione-S-transferases (gst-4 and gst-10; each p<0.005). Aspirin, and to a lesser degree salicylate, improved survival of hydrogen peroxide, and in the absence of exogenous stress aspirin extended lifespan by 21%-23% (each p<10(-9)), while salicylate added 14% (p<10(-6)). Aspirin and salicylate delayed age-dependent declines in motility and pharyngeal pumping (each p<0.005), and decreased intracellular protein aggregation (p<0.0001)-all established markers of physiological aging-consistent with slowing of the aging process. Aspirin fails to improve stress resistance or lifespan in nematodes lacking DAF-16, implying that it acts through this FOXO transcription factor., Innovation: Studies in mice and humans suggest that aspirin may protect against multiple age-associated diseases by reducing all-cause mortality. We now demonstrate that aspirin markedly slows many measures of aging in the nematode., Conclusions: Aspirin treatment is associated with diminished endogenous oxidant stress and enhanced resistance to exogenous peroxide, both likely mediated by activation of antioxidant defenses. Our evidence indicates that aspirin attenuates insulin-like signaling, thus protecting against oxidative stress, postponing age-associated functional declines and extending C. elegans lifespan under benign conditions.

Cardiac fibroblasts play a pivotal role in cardiac remodeling. In response to various pro-fibrotic stimuli, such as pro-inflammatory cytokines, anoxia-reoxygenation and pressure overload as well as aging, cardiac fibroblasts undergo proliferation, migration and activation, leading to the accumulation of extracellular matrix components and increased thickness and stiffness of heart. The ligands for peroxisome proliferator-activated receptor γ, especially thiazolidinediones, modulate the function of cardiac fibroblasts and the progression of cardiac remodeling, especially under pathological conditions. Unfortunately these agents have not been found to be consistently beneficial in heart failure. Although the precise intracellular signaling pathways are not fully understood, existing evidence strongly supports the involvement of oxidative stress and related signaling pathways. Further, peroxisome proliferator-activated receptor γ and lectin-like oxidized low-density lipoprotein receptor-1 together play critical roles in thiazolidinediones-modulated cardiac fibroblast dysfunction.

Objective: To investigate whether the protection of ischemic preconditioning (IPC) against myocardial ischemia/reperfusion (I/R) injury is mediated by toll-like receptor 4 (TLR4)/NF-κB pathway, and whether these effects are related to the release of calcitonin gene-related peptide (CGRP)., Methods: Sprague-Dawley rats were subjected to 60 min of ligation of the left anterior descending coronary artery followed by 3 h of reperfusion to induce I/R injury. IPC was performed by 4 cycles of 3-min left coronary artery occlusion followed by 5-min reperfusion before the I/R. The expression of TLR4 mRNA was determined by RT-PCR. TLR4 and NF-κB protein expression were analyzed by immunohistochemistry. Myocardial infarct size, CGRP concentration in plasma and activity of creatine kinase in serum were also measured., Results: IPC significantly reduced the infarct size and creatine kinase activity concomitantly with the increase in plasma CGRP concentration. The expressions of TLR4 protein and mRNA and NF-κB protein were increased by myocardial I/R injury, and dramatically inhibited by IPC., Conclusion: IPC protects against myocardial I/R injury by inhibition of TLR4/NF-κB pathway. These effects are related to the increased the release of CGRP.

We studied the gene expression profile during cardiac hypertrophy induced by angiotensin (ANG) II in wild-type mice and the influence of LOX-1 deletion on the gene expression profile. Wild-type and LOX-1 knockout mice were given saline or ANG II infusion for 4 wk. The saline-treated LOX-1 knockout mice showed upregulation of several genes including Ddx3y and Eif2s3y. ANG II infusion enhanced expression of genes known to be associated with cardiac remodeling, such as Agt, Ace, Timp4, Fstl, and Tnfrst12a, as well as oxidant stress-related genes Gnaq, Sos1, and Rac1. Some other strongly upregulated genes identified in this study have not been previously associated with LOX-1 deletion and/or hypertension. To confirm these observations with ANG II infusion and LOX-1 deletion, cultured HL-1 mouse cardiomyocytes were exposed to ANG II or transfected with pCI-neo/LOX-1, which resulted in severalfold increase in reactive oxygen species generation, upregulation of ANG II type 1 (AT(1)) receptor, and cardiomyocyte growth. Quantitative PCR analysis of these treated cardiomyocytes confirmed upregulation of many of the genes identified in the in vivo study. This study provides the first set of data on the gene expression profiling of cardiac tissue treated with ANG II and expands on the important role of LOX-1 in cardiac response to ANG II.

Many studies indicate that traditional Chinese herbs are beneficial in the prevention and treatment of cardiovascular diseases. Evodia rutaecarpa ('Wu-Chu-Yu') remains the most popular and multi-purpose herb traditionally used in China for treatment of headache, abdominal pain, postpartum hemorrhage, dysentery and amenorrhea. Rutaecarpine is one of the intriguing indolopyridoquinazoline alkaloids isolated from 'Wu-Chu-Yu'. Rutaecarpine has been shown to have cardiovascular biological effects such as inotropic and chronotropic, vasorelaxant, anti-platelet aggregation and anti-inflammatory effects. Furthermore, it has been reported that rutaecarpine has beneficial effects on some cardiovascular diseases. This review summarizes data on the cardiovascular pharmacological actions of rutaecarpine the published over the recent years, aiming to provide more evidence supporting its use in the treatment of cardiovascular diseases.