Qinqin Lin
Xi'an Jiaotong University
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Featured researches published by Qinqin Lin.
Journal of Ethnopharmacology | 2010
Hui Zhang; Weirong Wang; Rong Lin; Jiye Zhang; Qiaoli Ji; Qinqin Lin; Lina Yang
ETHNOPHARMACOLOGICAL RELEVANCE Qi deficiency and blood stasis is traditional Chinese medicine (TCM) syndrome. It leads to many diseases including coronary heart diseases (CHD) and cerebrovascular diseases (CVD). Inflammatory biomarkers and many endothelium-derived vasoactive factors are considered to play pivotal roles in CHD. Buyang Huanwu decoction (BYHWD), a TCM formula, has been recognized as a treatment for CHD with Qi deficiency and blood stasis syndrome and CVD in clinic. The mechanisms of BYHWD effect on CHD with Qi deficiency and blood stasis syndrome are unclear. AIM OF THE STUDY The aim is to investigate whether the effects of BYHWD on CHD with Qi deficiency and blood stasis syndrome in rats are associated with the inhibition of CRP, CD40 and vascular endothelial regulators. MATERIALS AND METHODS The treated groups were lavaged with 25.68, 12.84 and 6.42 g/kg BYHWD respectively once a day for 21 days. The level of C-reactive protein (CRP) in serum and the expression of cluster of differentiation 40 (CD40) in the heart and aorta of rats were detected. Moreover, the levels of thromboxaneA(2) (TXA(2)) and prostacyclin (PGI(2)) in plasma were measured and the levels of inducible nitric oxide synthase (iNOS) and endothelial nitric oxide synthase (eNOS) in serum were detected. RESULTS BYHWD (25.68 g/kg) significantly decreased the level of CRP in serum and BYHWD (25.68 and 12.84 g/kg) decreased the expression of CD40 in the heart and aorta (P<0.01). The results also revealed that BYHWD (25.68 g/kg) inhibited the levels of iNOS in serum and TXA(2) in plasma and increased the levels of eNOS in serum and PGI(2) in plasma (P<0.01). CONCLUSION The study shows that the ameliorative effects of BYHWD on CHD with Qi deficiency and blood stasis syndrome in rats are associated with the inhibition of CRP and CD40 and the regulation of endothelium-derived vasoactive factors.
Apoptosis | 2013
Weirong Wang; Chunfang Yan; Jiye Zhang; Rong Lin; Qinqin Lin; Lina Yang; Feng Ren; Jianfeng Zhang; Meixi Ji; Yanxiang Li
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.
Cytokine | 2012
Qinqin Lin; Chunfang Yan; Rong Lin; Jiye Zhang; Weirong Wang; Lina Yang; Kai-Fan Zhang
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.
Cellular Physiology and Biochemistry | 2012
Lina Yang; Jiye Zhang; Chunfang Yan; Jun Zhou; Rong Lin; Qinqin Lin; Weirong Wang; Kai-Fan Zhang; Guangde Yang; Xiao-Li Bian; Aiguo Zeng
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.
Toxicology in Vitro | 2012
Qiaoli Ji; Lina Yang; Jun Zhou; Rong Lin; Jiye Zhang; Qinqin Lin; Weirong Wang; Kai-Fan Zhang
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.
Evidence-based Complementary and Alternative Medicine | 2011
Guangde Yang; Zhiyuan Fang; Yu Liu; Hui Zhang; Xiaolian Shi; Qiaoli Ji; Qinqin Lin; Rong Lin
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.
Journal of Ethnopharmacology | 2011
Weirong Wang; Rong Lin; Hui Zhang; Qinqin Lin; Lina Yang; Kai-Fan Zhang; Feng Ren
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.
Toxicology in Vitro | 2010
Qiaoli Ji; Xiaolian Shi; Rong Lin; Youhua Mao; Xiaogang Zhai; Qinqin Lin; Jiye Zhang
The hepatotoxicity induced by valproic acid (VPA) has been described in many clinical studies and the related mechanism has been partly elucidated. The objective of this study is to investigate the hepatotoxicity and its underlying mechanism of valproic acid on human hepatoma carcinoma cell line HepG2. The cell viability was evaluated by 3-(4,5-dimethyltyiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. The activities of alanine aminotransferase (ALT), aspartate aminotransferase (AST) and lactate dehydrogenase (LDH) in the medium were detected using spectrophotometry. The gene expressions of cytochrome P450 1 A1 (CYP1A1), ATP-binding cassette transporter G1 (ABCG1) and carnitine palmitoyltransferase 1 (CPT1A), related to lipid transport and fatty acid metabolism, were measured by quantitative real-time reverse transcriptase-PCR. Treatment with valproate sodium obviously decreased the viability of HepG2 cells, accompanied by the increased leakages of ALT, AST and LDH in a dose-dependent manner. Furthermore, the gene expressions of CYP1A1, ABCG1 and CPT1A were almost up-regulated in the treated groups. In conclusion, these data suggest that VPA-induced hepatotoxicity was critically enhanced with the elevation of valproate sodium, which may be correlated with up-regulated gene expressions of CYP1A1, ABCG1 and CPT1A.
Experimental Cell Research | 2013
Weirong Wang; Qinqin Lin; Rong Lin; Jiye Zhang; Feng Ren; Jianfeng Zhang; Meixi Ji; Yanxiang Li
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.
Evidence-based Complementary and Alternative Medicine | 2011
Yu Liu; Rong Lin; Xiaolian Shi; Zhiyuan Fang; Weirong Wang; Qinqin Lin; Jiye Zhang; Hui Zhang; Qiaoli Ji
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.