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| 1 | Influences of blood lipids on the occurrence and prognosis of hemorrhagic transformation after acute cerebral infarction: a case-control study of 732 patients显示文摘Background: To study the influence of blood lipid levels on hemorrhagic transformation(HT) and prognosis after acute cerebral infarction(ACI).Methods: Patients with ACI within 72 h of symptoms onset between January 1 st, 2015, and December 31 st, 2016, were retrospectively analyzed. Patients were divided into group A(without HT) and group B(HT). The outcomes were assessed after 3 months of disease onset using the modified Rankin Scale(m RS). An m RS score of 0–2 points indicated excellent prognosis, and an m RS score of 3–6 points indicated poor prognosis.Results: A total of 732 patients conformed to the inclusion criteria, including 628 in group A and 104 in group B. The incidence of HT was 14.2%, and the median onset time was 2 d(interquartile range, 1–7 d). The percentages of patients with large infarct size and cortex involvement in group B were 80.8% and 79.8%, respectively, which were both significantly higher than those in group A(28.7 and 33.4%, respectively). The incidence rate of atrial fibrillation(AF) in group B was significantly higher than that in group A(39.4% vs. 13.9%, P<0.001). The adjusted multivariate analysis results showed that large infarct size, cortex involvement and AF were independent risk factors of HT, while total cholesterol(TC) was a protective factor of HT(OR=0.359, 95% CI 0.136–0.944, P=0.038). With every 1 mmol/L reduction in normal TC levels, the risk of HT increased by 64.1%. The mortality and morbidity at 3 months in group B(21.2% and 76.7%, respectively) were both significantly higher than those in group A(8.0% and 42.8%, respectively). The adjusted multivariate analysis results showed that large infarct size(OR=12.178, 95% CI 5.390–27.516, P<0.001) was an independent risk factor of long-term unfavorable outcomes, whereas low-density lipoprotein cholesterol(LDL-C) was a protective factor(OR=0.538, 95% CI 0.300–0.964, P=0.037). With every 1 mmol/L reduction in normal LDL-C levels, the risk of an unfavorable outcome increased by 46.2%. Major therapies, including intravenous recombinant human tissue plasminogen activator(r TPA), intensive lipid-lowering statins and anti-platelets, were not significantly related to either HT or long-term, post-ACI poor prognosis.Conclusions: For patients with large infarct sizes, especially those with cortex involvement, AF, or lower levels of TC, the risk of HT might increase after ACI. The risk of a long-term unfavorable outcome in these patients might increase with a reduction in LDL-C. | Gang Lv Guo-Qiang Wang Zhen-Xi Xia Hai-Xia Wang Nan Liu Wei Wei Yong-Hua Huang Wei-Wei Zhang | 2019 | Military Medical Research2019，6，3： | 60 |
| 2 | Lipid homeostasis and the formation of macrophage-derived foam cells in atherosclerosis显示文摘Atherosclerosis is a chronic,inflammatory disorder characterized by the deposition of excess lipids in the arterial intima.The formation of macrophage-derived foam cells in a plaque is a hallmark of the development of atherosclerosis.Lipid homeostasis,especially cho-lesterol homeostasis,plays a crucial role during the formation of foam cells.Recently,lipid droplet-associated proteins,including PAT and CIDE family proteins,have been shown to control the development of athero-sclerosis by regulating the formation,growth,stabiliza-tion and functions of lipid droplets in macrophage-derived foam cells.This review focuses on the potential mechanisms of formation of macrophage-derived foam cells in atherosclerosis with particular emphasis on the role of lipid homeostasis and lipid droplet-associated proteins.Understanding the process of foam cell for-mation will aid in the future discovery of novel thera-peutic interventions for atherosclerosis. | Yuan Yuan Peng Li Jing Ye | 2012 | Protein & Cell2012，3，3： | 44 |
| 3 | 致病的概念和胆石病的治疗显示文摘 Gallstone disease(GD) is a chronic recurrent hepatobiliary disease,the basis for which is the impaired metabolism of cholesterol,bilirubin and bile acids,which is characterized by the formation of gallstones in the hepatic bile duct,common bile duct,or gallbladder.GD is one of the most prevalent gastrointestinal diseases with a substantial burden to health care systems.GD can result in serious outcomes,such as acute gallstone pancreatitis and gallbladder cancer.The epidemiology,pathogenesis and treatment of GD are discussed in this review.The prevalence of GD varies widely by region.The prevalence of gallstone disease has increased in recent years.This is connected with a change in lifestyle:reduction of motor activity,reduction of the physical load and changes to diets.One of the important benefits of early screening for gallstone disease is that ultrasonography can detect asymptomatic cases,which results in early treatment and the prevention of serious outcomes.The pathogenesis of GD is suggested to be multifactorial and probably develops from complex interactions between many genetic and environmental factors.It suggests that corticosteroids and oral contraceptives,which contain hormones related to steroid hormones,may be regarded as a model system of cholelithiasis development in man.The achievement in the study of the physiology of bile formation and the pathogenesis of GD has allowed expanding indications for therapeutic treatment of GD. | Vasiliy Ivanovich Reshetnyak | 2012 | World Journal of Hepatology2012，4，2： | 39 |
| 4 | Regulation of glucose and lipid metabolism in health and disease显示文摘Glucose and fatty acids are the major sources of energy for human body. Cholesterol, the most abundant sterol in mammals, is a key component of cell membranes although it does not generate ATP. The metabolisms of glucose, fatty acids and cholesterol are often intertwined and regulated. For example, glucose can be converted to fatty acids and cholesterol through de novo lipid biosynthesis pathways. Excessive lipids are secreted in lipoproteins or stored in lipid droplets. The metabolites of glucose and lipids are dynamically transported intercellularly and intracellularly, and then converted to other molecules in specific compartments. The disorders of glucose and lipid metabolism result in severe diseases including cardiovascular disease, diabetes and fatty liver. This review summarizes the major metabolic aspects of glucose and lipid, and their regulations in the context of physiology and diseases. | Ligong Chen Xiao-Wei Chen Xun Huang Bao-Liang Song Yan Wang Yiguo Wang | 2019 | Science China(Life Sciences)2019，62，11： | 40 |
| 5 | Gallstones in patients with liver cirrhosis:Incidence,etiology,clinical and therapeutical aspects显示文摘Gallstones occur in about one third of the patients having liver cirrhosis.Pigment gallstones are the most frequent type,while cholesterol stones represent about15%of all stones in cirrhotics.Increased secretion of unconjugated bilirubin,increased hydrolysis of conjugated bilirubin in the bile,reduced secretion of bile acids and phospholipds in bile favor pigment lithogenesis in cirrhotics.Gallbladder hypomotility also contributes to lithogenesis.The most recent data regarding risk factors for gallstones are presented.Gallstone prevalence increases with age,with a ratio male/female higher than in the general population.Chronic alcoholism,viral C cirrhosis,and non-alcoholic fatty liver disease are the underlying liver diseases most often associated with gallstones.Gallstones are often asymptomatic,and discovered incidentally.If asymptomatic,expectant management is recommended,as for asymptomatic gallstones in the general population.However,a closer follow-up of these patients is necessary in order to earlier treat symptoms or complications.For symptomatic stones,laparoscopic cholecystectomy has become the therapy of choice.Child-Pugh class and MELD score are the best predictors of outcome after cholecystectomy.Patients with severe liver disease are at highest surgical risk,therefore gallstone complications should be treated using noninvasive or minimally invasive procedures,until stabilization of the patient condition. | Monica Acalovschi | 2014 | World Journal of Gastroenterology2014，20，23： | 39 |
| 6 | Lipid metabolism reprogramming and its potential targets in cancer显示文摘Reprogramming of lipid metabolism is a newly recognized hallmark of malignancy.Increased lipid uptake,storage and lipogenesis occur in a variety of cancers and contribute to rapid tumor growth.Lipids constitute the basic struc-ture of membranes and also function as signaling molecules and energy sources.Sterol regulatory element-binding proteins(SREBPs),a family of membrane-bound transcription factors in the endoplasmic reticulum,play a central role in the regulation of lipid metabolism.Recent studies have revealed that SREBPs are highly up-regulated in various cancers and promote tumor growth.SREBP cleavage-activating protein is a key transporter in the trafficking and activation of SREBPs as well as a critical glucose sensor,thus linking glucose metabolism and de novo lipid synthesis.Targeting altered lipid metabolic pathways has become a promising anti-cancer strategy.This review summarizes recent progress in our understanding of lipid metabolism regulation in malignancy,and highlights potential molecu-lar targets and their inhibitors for cancer treatment. | Chunming Cheng Feng Geng Xiang Cheng Deliang Guo | 2018 | Cancer Communications2018，38，1： | 34 |
| 7 | Elimination of cholesterol in human endothelial cells显示文摘Eliminationofcholesterolinhumanendothelialcels.XiuRuijuan,DuanChonggao,LiHongwei,etal.InstituteofMicrocirculation,ChineseAcad... | Xiu Ruijuan, Duan Chonggao, Li Hongwei, et al. Institute of Microcirculation, Chinese Academy of Medical Sciences, Peking Union Medical College, Beijing 100005, China. | 1998 | Chinese Medical Journal1998，，1： | 26 |
| 8 | Epidemiology of age-related macular degeneration (AMD): associations with cardiovascular disease phenotypes and lipid factors显示文摘Age-related macular degeneration(AMD)is the leading cause of irreversible blindness in adults over 50 years old.Genetic,epidemiological,and molecular studies are beginning to unravel the intricate mechanisms underlying this complex disease,which implicate the lipid-cholesterol pathway in the pathophysiology of disease development and progression.Many of the genetic and environmental risk factors associated with AMD are also associated with other complex degenerative diseases of advanced age,including cardiovascular disease(CVD).In this review,we present epidemiological findings associating AMD with a variety of lipid pathway genes,cardiovascular phenotypes,and relevant environmental exposures.Despite a number of studies showing significant associations between AMD and these lipid/cardiovascular factors,results have been mixed and as such the relationships among these factors and AMD remain controversial.It is imperative that researchers not only tease out the various contributions of such factors to AMD development but also the connections between AMD and CVD to develop optimal precision medical care for aging adults. | Katie L.Pennington Margaret M.DeAngelis | 2016 | Eye and Vision2016，3，1： | 22 |
| 9 | Silymarin in non alcoholic fatty liver disease显示文摘AIM: This study was undertaken to evaluate the hepatic effects of silybum marianum on non alcoholic fatty liver disease (NAFLD). METHODS: In 72 patients affected by NAFLD, main metabolic, hepatic and anti-inflammatory parameters were assayed after 3 mo of a restricted diet and before silymarin treatment (twice a day orally). The brightness of liver echography texture (hepatorenal ratio brightness) was also defined at same time. These evaluations were repeated after 6 mo of treatment. RESULTS: Serum levels of some metabolic and anti-inflammatory data nonsignificantly lowered after 6 mo of silymarin. On the contrary, Steato test, alanine aminotransferase (ALT), aspartate aminotransferase (AST) and gamma-glutamyl transpeptidase were significantly (P < 0.001) reduced. Instead, the AST/ALT ratio unchanged. Finally, the hepatorenal brightness ratio, as an index of hepatic steatosis, significantly (P < 0.05) dropped. CONCLUSION: The obtained results indicate that silymarin appears to be effective to reduce the biochemical, inflammatory and ultrasonic indices of hepatic steatosis. Some parameters indicative of early stage of atherosclerosis were also lowered. | Fulvio Cacciapuoti Anna Scognamiglio Rossella Palumbo Raffaele Forte Federico Cacciapuoti | 2013 | World Journal of Hepatology2013，5，3： | 17 |
| 10 | Ursodeoxycholic acid therapy in gallbladder disease,a story not yet completed显示文摘Gallstone disease represents an important issue in the healthcare system.The principal non-invasive nonsurgical medical treatment for cholesterol gallstones is still represented by oral litholysis with bile acids.The first successful and documented dissolution of cholesterol gallstones was achieved in 1972.Since then a large number of investigators all over the world,have been dedicated in biochemical and clinical studies on ursodeoxycholic acid(UDCA),demonstrating its extreme versatility.This editorial is aimed to provide a brief review of recent developments in UDCA use,current indications for its use and,the more recent advances in understanding its effects in terms of an antiinflammatory drug. | Michele Pier Luca Guarino Silvia Cocca Annamaria Altomare Sara Emerenziani Michele Cicala | 2013 | World Journal of Gastroenterology2013，19，31： | 16 |
| 11 | Association of serum lipid levels with diabetic retinopathy显示文摘AIM: To assess the association between serum lipids and diabetic retinopathy (DR). · METHODS: Sixty -one diabetic patients without retinopathy (NDR), 55 diabetic patients with non - proliferative retinopathy (NPDR) and 75 diabetic patients with proliferative retinopathy (PDR) according to ETDRS grading scale were enrolled in this study. Total cholesterol, high density lipoprotein (HDL), low density lipoprotein (LDL), very low density lipoprotein (VLDL) and triglyceride values were compared between the groups. ·RESULTS: The groups were well-balanced in terms of age and gender (P =0.071, P =0.265 respectively). The mean HbA1c values were significantly lower in NDR group than the NPDR and PDR groups(P =0.004, P =0.009 respectively). Mean total cholesterol, triglyceride, LDL, HDL and VLDL levels were not significantly different between the groups (P =0.693, P =0.774, P =0.644, P = 0.910 and P =0.967 respectively, one way ANOVA). Mean total cholesterol, triglyceride, LDL, HDL and VLDL levels were not significantly different between the patients with ME and patients without ME(P =0.622, P =0.113, P =0.955, P =0.735 and P =0.490 respectively, t -test). The mean blood glucose significantly correlated with total cholesterol (r =0.173, P =0.017) and LDL (r =0.190, P = 0.008). The mean HbA1c significantly correlated with total cholesterol (r =0.158, P =0.030) and triglyceride (r =0.148, P =0.042). ·CONCLUSION: Serum lipid levels were not significantly associated with the severity of DR or existence of ME despite the significant correlation between the mean blood glucose, HbA1c and total cholesterol. | Ebru Nevin Cetin Yunus Bulgu Seyfullah Ozdemir Senay Topsakal Fulya Akln Hulya Aybek Cem Ylldlrlm | 2013 | International Journal of Ophthalmology(English edition)2013，6，3： | 14 |
| 12 | 下肢动脉硬化闭塞症诊治指南(下)显示文摘<正>3治疗3.1针对心血管危险因素的治疗3.1.1降脂药物治疗建议所有下肢动脉硬化闭塞症(atherosclerosis obliterans,ASO)患者使用他汀类药物降脂治疗~[1]。他汀类药物主要适用于血中总胆固醇及低密度脂蛋白胆固醇(low density lipoprotein cholesterol,LDL-C)增高为主的患者。以多项随机对照试验研究结果为依据。 | | 2015 | 中国血管外科杂志(电子版)2015，7，4： | 14 |
| 13 | Aloe-emodin exerts cholesterol-lowering effects by inhibiting proprotein convertase subtilisin/kexin type 9 in hyperlipidemic rats显示文摘Hyperlipidemia(HPL)characterized by metabolic disorder of lipids and cholesterol is one of the important risk factors for cardiovascular diseases.Proprotein convertase subtilsin/kexin type 9(PCSK9)is a potent circulating regulator of LDL through its ability to induce degradation of the low-density lipoprotein cholesterol receptor(LDLR)in the lysosome of hepatocytes.Aloe-emodin(AE)is one of potentially bioactive components of Chinese traditionalmedicine Daming capsule.In this study we evaluated the HPL-lowering efficacy of AE in both in vivo and in vitro HPL models.High-fat diet-induced rats were treated with AE(100 mg/kg per day,ig)for 6 weeks.We found that AE administration significantly decreased the levels of total cholesterol(TC)and LDL in the serum and liver tissues.Moreover,AE administration ameliorated HPL-induced hepaticlipid aggregation.But AE administration did not significantly inhibit HMG-CoA reductase activity in the liver of HPL rats.A cellular model of HPL was established in human hepatoma(HepG2)cells treated with cholesterol(20 μg/mL)and 25-hydroxycholesterol(2 μg/mL),which exhibited markedly elevated cholesterol levels.The increased cholesterol levels could be reversed by subsequent treatment with AE(30 μM).In both the in vivo and in vitro HPL models,we revealed that AE selectively suppressed the stero-regulatory element-binding protein-2(SREBP-2)and hepatocyte nuclear factor(HNF)1α-mediated PCSK9 signaling,which in turn upregulated LDL receptor(LDLR)and promoted LDL uptake.This study demonstrates that AE reduces cholesterol content in HPL rats by inhibiting the hepatic PCSK9/LDLR pathway. | Zhen-li Su Peng-zhou Hang Juan Hu Yu-yang Zheng Han-qi Sun Jing Guo Ke-yu Liu Zhi-min Du | 2020 | Acta Pharmacologica Sinica2020，41，8： | 14 |
| 14 | Beneficial Effects of Oolong Tea Consumption on Diet-induced Overweight and Obese Subjects显示文摘Objective:To determine the anti-obesity effects of oolong tea on diet-induced overweight or obesity.Methods:A total of 8 g of oolong tea a day for 6 weeks was ingested by 102 diet-induced overweight or obese subjects.The body fat level of the subjects was determined at the same time by taking body weight, height and waist measurements.The thickness of the subcutaneous fat layer was also determined on the abdomen 3 cm to the right of the navel by the ultrasonic echo method.On the other hand,effects of ool... | 何蓉蓉 陈玲 林炳辉 松井阳吉 姚新生 栗原博 | 2009 | Chinese Journal of Integrative Medicine2009，15，1： | 13 |
| 15 | Scavenger receptor BI: A multi-purpose player in cholesterol and steroid metabolism显示文摘Scavenger receptor class B type Ⅰ (SR-BI) is an important member of the scavenger receptor family of integral membrane glycoproteins. This review highlights studies in SR-BI knockout mice, which concern the role of SR-BI in cholesterol and steroid metabolism. SR-BI in hepatocytes is the sole molecule involved in selective uptake of cholesteryl esters from high-density lipoprotein (HDL). SR-BI plays a physiological role in binding and uptake of native apolipoprotein B (apoB)-containing lipoproteins by hepatocytes, which identif ies SR-BI as a multipurpose player in lipid uptake from the blood circulation into hepatocytes in mice. In adrenocortical cells, SR-BI mediates the selective uptake of HDL-cholesteryl esters, which is eff iciently coupled to the synthesis of glucocorticoids (i.e. corticosterone). SR-BI knockout mice suffer from adrenal glucocorticoid insuff iciency, which suggests that functional SR-BI protein is necessary for optimal adrenal steroidogenesis in mice. SR-BI in macrophages plays a dual role in cholesterol metabolism as it is able to take up cholesterol associated with HDL and apoBcontaining lipoproteins and can possibly facilitate cholesterol efflux to HDL. Absence of SR-BI is associated with thrombocytopenia and altered thrombosis susceptibility, which suggests a novel role for SR-BI in regulating platelet number and function in mice. Transgenic expression of cholesteryl ester transfer protein in humanized SR-BI knockout mice normalizes hepatic delivery of HDL-cholesteryl esters. However, other pathologies associated with SR-BI def iciency, i.e. increased atherosclerosis susceptibility, adrenal glucocorticoid insuffi ciency, and impaired platelet function are not normalized, which suggests an important role for SR-BI in cholesterol and steroid metabolism in man. In conclusion, generation of SR-BI knockout mice has signif icantly contributed to our knowledge of the physiological role of SR-BI. Studies using these mice have identif ied SR-BI as a multi-purpose player in cholesterol and steroid metabolism because it has distinct roles in reverse cholesterol transport, adrenal steroidogenesis, and platelet function. | Menno Hoekstra Theo JC Van Berkel Miranda Van Eck | 2010 | World Journal of Gastroenterology2010，16，47： | 11 |
| 16 | Metabolic syndrome in hypertensive patients:An unholy alliance显示文摘For many years, it has been recognized that hypertension tends to cluster with various anthropometric and metabolic abnormalities including abdominal obesity, elevated triglycerides, reduced high-density lipoprotein cholesterol, glucose intolerance, insulin resistance and hyperuricemia. This constellation of various conditions has been transformed from a pathophysiological concept to a clinical entity, which has been defined metabolic syndrome(MetS). The consequences of the MetS have been difficult to assess without commonly accepted criteria to diagnose it. For this reason, on 2009 the International Diabetes Federation, the American Heart Association and other scientific organizations proposed a unified MetS definition. The incidence of the MetS has been increasing worldwide in parallel with an increase in overweight and obesity. The epidemic proportion reached by the MetS represents a major public health challenge, because several lines of evidence showed that the MetS, even without type 2 diabetes, confers an increased risk of cardiovascular morbidity and mortality in different populations including also hypertensive patients. It is likely that the enhanced cardiovascular risk associated with MetS in patients with high blood pressure may be largely mediated through an increased prevalence of preclinical cardiovascular and renal changes, such as left ventricular hypertrophy, early carotid atherosclerosis, impaired aortic elasticity, hypertensive retinopathy and microalbuminuria. Indeed, many reports support this notion, showing that hypertensive patients with MetS exhibit, more often than those without it, these early signs of end organ damage, most of which are recognized as significant independent predictors of adverse cardiovascular outcomes. | Giuseppe Mulè IIenia Calcaterra Emilio Nardi Giovanni Cerasola Santina Cottone | 2014 | World Journal of Cardiology2014，6，9： | 10 |
| 17 | MicroRNA-185-5p mediates regulation of SREBP2 expression by hepatitis C virus core protein显示文摘AIM: To investigate the molecular mechanism for regulation of cholesterol metabolism by hepatitis C virus(HCV) core protein in Hep G2 cells.METHODS: HCV genotype 1b core protein was cloned and expressed in Hep G2 cells. The cholesterol content was determined after transfection. The expression of sterol regulatory element binding protein 2(SREBP2) and the rate-limiting enzyme in cholesterol synthesis(HMGCR) was measured by quantitative real-time PCR and immunoblotting after transfection. The effects of core protein on the SREBP2 promoter and 3'-untranslated region were analyzed by luciferase assay. We used different target predictive algorithms, micro RNA(mi RNA) mimics/inhibitors, and site-directed mutation to identify a putative target of a particular mi RNA.RESULTS: HCV core protein expression in Hep G2 cells increased the total intracellular cholesterol level(4.05 ± 0.17 vs 6.47 ± 0.68, P = 0.001), and this increase corresponded to an increase in SREBP2 and HMGCR m RNA levels(P = 0.009 and 0.037, respectively) and protein expression. The molecular mechanism studyrevealed that the HCV core protein increased the expression of SREBP2 by enhancing its promoter activity(P = 0.004). In addition, mi R-185-5p expression was tightly regulated by the HCV core protein(P = 0.041). Moreover, overexpression of mi R-185-5p repressed the SREBP2 m RNA level(P = 0.022) and protein expression. In contrast, inhibition of mi R-185-5p caused upregulation of SREBP2 protein expression. mi R-185-5p was involved in the regulation of SREBP2 expression by HCV core protein. CONCLUSION: HCV core protein disturbs the cholesterol homeostasis in Hep G2 cells via the SREBP2 pathway; mi R-185-5p is involved in the regulation of SREBP2 by the core protein. | Min Li Qi Wang Shun-Ai Liu Jin-Qian Zhang Wei Ju Min Quan Sheng-Hu Feng Jin-Ling Dong Ping Gao Jun Cheng | 2015 | World Journal of Gastroenterology2015，21，15： | 10 |
| 18 | Effects of sphincter of Oddi motility on the formation of cholesterol gallstones显示文摘AIM: To investigate the mechanisms and effects of sphincter of Oddi(SO) motility on cholesterol gallbladder stone formation in guinea pigs.METHODS: Thirty-four adult male Hartley guinea pigs were divided randomly into two groups, the control group(n = 10) and the cholesterol gallstone group(n = 24), which was sequentially divided into four subgroups with six guinea pigs each according to time of sacrifice. The guinea pigs in the cholesterol gallstone group were fed a cholesterol lithogenic diet and sacrificed after 3, 6, 9, and 12 wk. SO manometry and recording of myoelectric activity were obtained by a multifunctional physiograph at each stage. Cholecystokinin-A receptor(CCKAR) expression levels in SO smooth muscle were detected by quantitative real-time PCR(q RT-PCR) and serum vasoactive intestinal peptide(VIP), gastrin, and cholecystokinin octapeptide(CCK-8) were detected by enzyme-linked immunosorbent assay at each stage in the process of cholesterol gallstone formation.RESULTS: The gallstone formation rate was 0%, 0%, 16.7%, and 83.3% in the 3, 6, 9, and 12 wk groups, respectively. The frequency of myoelectric activity in the 9 wk group, the amplitude of myoelectric activity in the 9 and 12 wk groups, and the amplitude and the frequency of SO in the 9 wk group were all significantly decreased compared to the control group. The SO basal pressure and common bile duct pressure increased markedly in the 12 wk group, and the CCKAR expression levels increased in the 6 and 12 wk groups compared to the control group. Serum VIP was elevated significantly in the 9 and 12 wk groups and gastrin decreased significantly in the 3 and 9 wk groups. There was no difference in serum CCK-8 between the groups.CONCLUSION: A cholesterol gallstone-causing diet can induce SO dysfunction. The increasing tension of the SO along with its decreasing activity may play an important role in cholesterol gallstone formation. Expression changes of CCKAR in SO smooth muscle and serum VIP and CCK-8 may be important causes of SO dysfunction. | Zhong-Hou Rong Hong-Yuan Chen Xin-Xing Wang Zhi-Yi Wang Guo-Zhe Xian Bang-Zhen Ma Cheng-Kun Qin Zhen-Hai Zhang | 2016 | World Journal of Gastroenterology2016，22，24： | 10 |
| 19 | Photoresponsive organogel and organized nanostructures of cholesterol imide derivatives with azobenzene substituent groups | Tifeng Jiao Yujin Wang Fengqing Gao Jingxin Zhou Faming Gao | 2012 | Progress in Natural Science:Materials International2012，22，1： | 9 |
| 20 | Mitochondrial function and regulation of macrophage sterol metabolism and inflammatory responses显示文摘The aim of this review is to explore the role of mitochondria in regulating macrophage sterol homeostasis and inflammatory responses within the aetiology of atherosclerosis.Macrophage generation of oxysterol activators of liver X receptors(LXRs),via sterol 27-hydroxylase,is regulated by the rate of flux of cholesterolto the inner mitochondrial membrane,via a complex of cholesterol trafficking proteins.Oxysterols are key signalling molecules,regulating the transcriptional activity of LXRs which coordinate macrophage sterol metabolism and cytokine production,key features influencing the impact of these cells within atherosclerotic lesions.The precise identity of the complex of proteins mediating mitochondrial cholesterol trafficking in macrophages remains a matter of debate,but may include steroidogenic acute regulatory protein and translocator protein.There is clear evidence that targeting either of these proteins enhances removal of cholesterol via LXRα-dependent induction of ATP binding cassette transporters(ABCA1,ABCG1) and limits the production of inflammatory cytokines; interventions which influence mitochondrial structure and bioenergetics also impact on removal of cholesterol from macrophages.Thus,molecules which can sustain or improve mitochondrial structure,the function of the electron transport chain,or increase the activity of components of the protein complex involved in cholesterol transfer,may therefore have utility in limiting or regressing atheroma development,reducing the incidence of coronary heart disease and myocardial infarction. | Annette Graham Anne-Marie Allen | 2015 | World Journal of Cardiology2015，7，5： | 9 |
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