2'-,5'-Oligoadenylate synthetase response ratio predicting virological response to PEG-interferon-alpha2b plus ribavirin therapy in patients with chronic hepatitis C

OBJECTIVE: Although all the mechanisms of elimination of hepatitis C virus (HCV) by Interferon (IFN) have not been fully elucidated, the 2'-5'-oligoadenylate (2-5A) system is one of the mechanisms of the antiviral effect of IFN. Consequently, the measurement of 2'-5'-oligoadenylate synthetase (2-5AS) activity could be useful for the evaluation of IFN treatment. This retrospective study was aimed at assessing whether 2-5AS activity functions as a clinical marker of virological response to PEG-interferon-alpha2b (PEG-IFN) plus ribavirin therapy of chronic hepatitis C. METHODS: The 32 patients included in this study had high viral loads of serum HCV-RNA of genotype 1b with chronic hepatitis C. All the patients received a regimen of PEG-IFN plus ribavirin for 48 weeks, and were then divided into two groups: one group (effective group) with undetectable serum HCV-RNA levels at 24 weeks (n = 22) of therapy, the other group (ineffective group) with persistent presence of HCV-RNA in serum at 24 weeks (n = 10). The 2-5AS activity in serum was measured 2, 8 and 12 weeks before initial administration. RESULTS: The 2-5AS response ratio (measured value/measured value of baseline 2-5AS) at 2, 8 and 12 weeks after the administration in the effective group was significantly higher than that in the ineffective group. CONCLUSIONS: These results suggest that the ratio of 2-5AS is closely related to the antiviral effect, and that the measurement of 2-5AS response ratio may be a useful clinical parameter of virological response to PEG-IFN plus ribavirin therapy of chronic hepatitis C.     

Pain-reducing anesthesia prevents oxidative stress in human term placenta

Anesthesia is sometimes used for the reduction of maternal pain in normal human term labor, but whether the drugs affect oxidative stress remains unclear. The placenta serves as an interface between the maternal and fetal vasculature. In this study, we immunohistochemically analyzed two markers for oxidative stress, namely 8-hydroxy-2''-deoxyguanosine (8-OHdG) and 4-hydroxy-2-nonenal–modified proteins (HNE), using placentas from 21 cases of normal tansvaginal delivery (V group), 20 Caesarean sections (C group), and 17 normal transvaginal deliveries with epidural anesthesia (E group). 8-OHdG staining in the nuclei of trophoblasts lining the chorionic villi was significantly stronger in the V group either compared with the C or E group (p<0.001), without significant differences in the C and E groups (p = 0.792). Moderate to intense staining by HNE of the intravascular serum of chorionic villi vasculature was frequently observed in the placentas from the V group, but less frequently of those in either C or E groups (p<0.001), nor the p value comparing the C and E groups was significant (p = 0.128) for HNE staining. Our results suggest that although the role of oxidative stress and its influences on fetal state in the placenta in labor remains unclear, it seems to be lessened by epidural anesthesia.     

Bile acid metabolism in heterozygous familial hypercholesterolaemia: a study comparing affected and unaffected siblings of four kindreds

Previous studies have indicated that quantitative as well as qualitative abnormalities of bile acid metabolism frequently occur in hypercholesterolaemia. In order to determine if this is a feature of familial hypercholesterolaemia, bile acid kinetics and biliary lipid composition were determined in 15 affected (heterozygous) and six unaffected siblings of four kindreds with familial hypercholesterolaemia. Furthermore, serum levels of cholic acid, chenodeoxycholic acid and deoxycholic acid were measured with a mass fragmentographic technique in 15 members of two of the kindreds, and secretion rates of biliary lipids were measured in six members of two kindreds. No differences with regard to these parameters between affected and unaffected siblings could be detected. There was a close resemblance between relatives of a given kindred concerning bile acid pool size and serum bile acid levels. No evidence for a defective bile acid metabolism in familial hypercholesterolaemia could be gained from the present study. It is concluded that the deficient receptor-mediated elimination of low density lipoprotein cholesterol in this disorder does not influence the maintenance of normal bile acid metabolism.     

Roles of oxidative stress in stomach disorders

The stomach is a sensitive digestive organ that is susceptible and exposed to exogenous pathogens from the diet. In response to such pathogens, the stomach induces oxidative stress, which might be related to the development of gastric organic disorders such as gastritis, gastric ulcers, and gastric cancer, as well as functional disorders such as functional dyspepsia. In particular, the bacterium Helicobacter pylori plays a major role in eliciting and confronting oxidative stress in the stomach. The present paper summarizes the pathogenesis of oxidative stress in the stomach during the development of various stomach diseases.     

Simulation of the metabolism and enterohepatic circulation of endogenous chenodeoxycholic acid in man using a physiological pharmacokinetic model

The metabolism and enterohepatic circulation of chenodeoxycholic acid (CDC), a major primary bile acid in man, has been stimulated using a multicompartmental physiological pharmacokinetic model which was previously reported and used to simulate the metabolism of cholic acid. The model features compartments and linear transfer coefficients. Compartments, which are defined as the pools of single chemical species in well defined anatomical volumes, are aggregated into nine 'spaces' based on anatomical and physiological considerations (liver, gall-bladder, bile ducts, duodeno-jejunum, ileum, colon, portal blood, sinusoidal blood, and general circulation). Each space contains several compartments which correspond to the compounds present in that space, for example, the compound in question and its biotransformation products. For CDC (as for cholic acid in the previous simulation) each space contains three compartments corresponding to the unconjugated bile acid, its glycine amidate, and its taurine amidate. Transfer coefficients, which denote the fractional amount of the compartment's contents exiting per unit time, are categorized according to function: flow, for example gall-bladder contraction (which involves transfer of all substances contained in the space at the same fractional rate); biotransformation (which transfers the substrate from one compartment to another within the same space); or transport (which denotes movements between contiguous compartments, belonging to different spaces across a diffusion membrane or a cellular barrier). The model is made time-dependent by incorporating meals which trigger gall-bladder emptying and modify intestinal flow. The transfer coefficients in the cholic acid model were modified for the CDC model since there is indirect evidence that CDC amidates (probably chenodeoxycholylglycine) are absorbed from the duodeno-jejunum and the first pass hepatic clearance of CDC species differs from that of cholyl species. The model was then used with all existing experimental data to simulate CDC metabolism in healthy humans over a 24-h period during which three meals were ingested. Satisfactory agreement was obtained between simulated and experimental data indicating that this model continues to be useful for describing the metabolism of bile acids and may also be of value for describing the metabolism of drugs whose metabolism is similar to that of bile acids.     

Dietary chlorogenic acid ameliorates oxidative stress and improves endothelial function in diabetic mice via Nrf2 activation

ObjectivesChlorogenic acid (CGA) is an antioxidant dietary factor. We investigated the effects of CGA on endothelial cell dysfunction in diabetic mice and the mechanistic role of nuclear factor erythroid-related factor 2 (Nrf2) in the antioxidant effect of CGA.MethodsDiabetic (db/db) mice were fed normal chow or chow containing 0.02% CGA for 12 weeks. Human umbilical vein endothelial cells (HUVECs) and mouse aortas were treated with normal or high glucose.ResultsCGA treatment induced upregulation of Nrf2 in HUVECs in a dose-dependent manner. CGA pretreatment prevented reactive oxygen species generation and preserved nitric oxide bioavailability in HUVECs and aortas from wild-type but not Nrf2^−/− mice. CGA improved endothelium-dependent relaxation in high glucose-treated aortas from wild-type and db/db mice, but not Nrf2^−/− mice. Dietary CGA improved endothelium-dependent relaxation in db/db mice.ConclusionsCGA ameliorates endothelial dysfunction in diabetic mice through activation of the Nrf2 anti-oxidative pathway.     

Bile acid content of gallbladder bile and stones in type lib and IV hyperlipoproteinemia

We examined the bile acid composition of gallbladder bile using reversed-phase high performance liquid chromatography (HPLC), in normolipemic and hyperlipidemic (types IIb and IV) patients with cholelithiasis and compared them with normal subjects. Similarly, bile acid composition was determined in the gallstones of these patients.No free bile acids were found in any of the samples examined. We observed that gallbladder bile and gallstones of patients with type IV hyperlipidemia showed a significant increase in the percentage of glyco-conjugated bile acids and reduction in taurine conjugates.Based on this finding we postulate that in addition to biliary lipid composition bile acid composition may also play a role in the pathogenesis of cholesterol gallstone formation.     

Serum calcineurin activity in relation to oxidative stress and glycemic control in type II diabetes mellitus

OBJECTIVES: In view of the well-recognized prevalence of oxidative stress in diabetes mellitus and the susceptibility of calcineurin (Ca(2+)-calmodulin dependent protein phosphatase 2 B) to free radicals, calcineurin was assayed in the sera of type II diabetic patients. DESIGN AND METHODS: Serum contents of thiobarbituric acid reactive substances, calcineurin and calmodulin, as well as activities of calcineurin and superoxide dismutase were measured in 81 diabetic patients and compared with age-matched controls. RESULTS: Oxidative stress in diabetic subjects was evidenced by increased thiobarbituric acid reactive substances, decreased superoxide dismutase activity concomitant with decreased calcineurin activity in sera. The observed decrease in calcineurin activity had a reciprocal correlation with fasting blood sugar, thiobarbituric acid reactive substances, and glycosylated hemoglobin. CONCLUSION: The inverse correlation observed between serum calcineurin activity and glycosylated hemoglobin levels suggests that an assay of serum calcineurin activity may be useful in simultaneous assessment of oxidative stress and glycemic control in type II diabetes mellitus.     

糖尿病前期患者晚期糖基化终末产物受体与氧化应激的关系

目的 通过测定糖耐量正常者、糖尿病前期及糖尿病患者血浆可溶性晚期糖基化终末产物受体(sRAGE)、内源性分泌型晚期糖基化终末产物受体(esRAGE)及氧化应激的水平,探讨糖尿病前期血浆sRAGE、esRAGE水平的变化与氧化应激的相关性,为深入了解糖尿病前期血管并发症的发病机制提供依据.方法 研究对象均行75 g标准口服葡萄糖耐量实验(OGTT)和胰岛素释放试验,按血糖水平分为糖耐量正常(NGT)组、糖尿病前期(Pre-DM)组、糖尿病(DM)组,采用酶联免疫吸附检测(ELISA)法检测血浆sRAGE、esRAGE、8-异前列腺素F2α(8-isoPGF2α);硫代巴比妥酸(TBA)法测定丙二醛(MDA),羟胺法测定超氧物岐化酶(SOD),比色法测定血浆总抗氧化能力(TAOC).结果 Pre-DM组和DM组的sRAGE、esRAGE、SOD水平明显低于NGT组,Pre-DM组和DM组的8-iso-PGF2α、MDA水平明显高于NGT组,差异均有统计学意义(P＜0.05);Pre-DM组和NGT组的TAOC水平明显高于DM组(P＜0.05);血浆esRAGE水平与sRAGE、TAOC呈正相关(r=0.39、0.64,P＜0.05),与MDA呈负相关(r =-0.45,P＜0.05),与年龄、体质量指数(BMI)、收缩压、舒张压、空腹血糖、空腹胰岛素、糖化血红蛋白、甘油三酯、低密度脂蛋白、高密度脂蛋白、8-iso PGF2α无明显相关性(P＜0.05).结论 糖尿病前期患者已发生sRAGE、esRAGE及氧化应激水平的改变,sRAGE、esRAGE在机体氧化应激与抗氧化防御平衡间可能发挥重要作用.     

Effect of tauroursodeoxycholic acid on bile acid-induced apoptosis in primary human hepatocytes

BACKGROUND/AIMS: The accumulation of endogenous bile acids contributes to hepatocellular damage during cholestatic liver disease. To evaluate the potential role of apoptotic cell death due to increased concentrations of bile acids, primary human hepatocytes were treated with hydrophobic and hydrophilic bile acids. Because the Fas receptor-ligand system may mediate apoptosis in human liver cells, the effect of toxic bile acids on hepatocellular Fas receptor expression was evaluated. MATERIALS AND METHODS: Primary human hepatocytes were incubated with 50 and 100 microM glycochenodeoxycholic acid (GCDCA) and co-incubated with equimolar concentrations of tauroursodeoxycholic acid (TUDCA). To evaluate cytolytic and apoptotic effects, morphological alterations, hepatocellular enzyme release, nuclear DNA fragmentation and hepatocellular Fas receptor expression were evaluated. RESULTS: Apoptotic cell death was significantly increased after exposure to 50 microM GCDCA. Bile acid-induced apoptosis was not accompanied by hepatocellular Fas receptor overexpression. Tauroursodeoxycholic acid reduced apoptosis, as indicated by a significant reduction of oligonucleosomal DNA cleavage. Fas receptor expression was not significantly affected by tauroursodeoxycholic acid. At higher concentrations, direct cytolytic cell destruction was observed. CONCLUSION: Primary human hepatocytes represent a suitable model to study bile acid-induced apoptotic cell death. In these hepatocytes, already low bile acid concentrations might induce apoptotic cell death, which is not triggered by hepatocellular Fas receptor overexpression. Apoptotic DNA fragmentation was significantly reduced by co-incubation with tauroursodeoxycholic acid. The reduction of bile acid-induced apoptosis by ursodeoxycholic acid and its conjugates may contribute to the beneficial effects of these hydrophilic bile acids used for medical treatment of several cholestatic liver diseases.     

Occurrence of cholesterol monohydrate crystals in gallbladder and hepatic bile in man: influence of bile acid treatment

The occurrence of cholesterol monohydrate crystals was examined and related to the degree of cholesterol saturation in gallbladder bile and hepatic bile of gallstone (GS) patients (n = 34), gallstone-free (GSF) subjects (n = 33) and GS patients treated with chenodeoxycholic acid (CDCA (n = 7) or ursodeoxycholic acid (UDCA) (n = 11) for 3 weeks prior to cholecystectomy. Twenty-five untreated GS patients (74%) and four UDCA-treated patients (40%) displayed cholesterol crystals in the gallbladder bile. Only two GSF subjects (6%) and none of the CDCA-treated patients had crystals. Half of the patients with crystals in the gallbladder bile had crystals also in the hepatic bile. Cholesterol saturation of the gallbladder bile was higher in GS (142 +/- 15%, mean +/- SEM) than in GSF patients (74 +/- 5%). Saturation was also higher in GS patients with crystals (157 +/- 20%) than in those without crystals (99 +/- 12%). Gallbladder bile was unsaturated in all CDCA- and UDCA-treated patients. The results underline the importance of the degree of cholesterol saturation for the formation of cholesterol crystals. The data also give further support to the concept that the mechanism for inducing gallstone dissolution is different for CDCA and UDCA.     

Exhaled markers of oxidative stress in idiopathic pulmonary fibrosis

BACKGROUND: Expired breath condensate (EBC) has never been used to explore the level of oxidative stress in idiopathic pulmonary fibrosis (IPF). Therefore, the aim of this study was to measure the levels of H2O2 and 8-isoprostane, as biomarkers of oxidative stress, in the EBC of patients with IPF. MATERIALS AND METHODS: We investigated 16 patients with IPF and 15 healthy subjects as the control group. The levels of H2O2 and 8-isoprostane were measured in the EBC of all subjects and were compared between the IPF and control groups. In patients with IPF, H2O2 and 8-isoprostane were further correlated with pulmonary function tests (PFTs), the resting pO2 and the differential cell count from the bronchoalveolar lavage fluid (BALF). RESULTS: The mean (95%CI) concentration of H2O2 was increased in the patients with IPF compared with the normal subjects (0.36, 0.24-0.47 microM vs. 0.16, 0.10-0.23 microM, P=0.003). The mean (95%CI) concentration of 8-isoprostane was also increased in the patients with IPF compared with the controls (74, 38-110 pg mL-1 vs. 33, 28-39 pg mL-1, P=0.02). In the patients with IPF, the diffusing capacity of the lung for carbon monoxide was negatively correlated with the levels of H2O2 in EBC (P=0.03, r=-0.58). No other correlation was found between the oxidative stress markers in the EBC and PFT values, pO2 or BALF cell count. CONCLUSIONS: Our data suggest that H2O2 and 8-isoprostane are increased in the EBC of patients with IPF. H2O2 may be correlated with the severity of the disease in IPF.     

抗氧化治疗对2型糖尿病患者氧化应激水平及炎症因子的影响

目的探讨α-硫辛酸与维生素C对2型糖尿病患者氧化应激水平及炎症因子影响。方法 60例2型糖尿病患者根据治疗方法不同分为α-硫辛酸组、维生素C组,各30例。60例患者均接受7d胰岛素强化降糖治疗,α-硫辛酸组,继续胰岛素强化治疗后给予α-硫辛酸治疗,维生素C组,继续胰岛素强化治疗后给予维生素C片治疗。检测2组患者血糖、糖化血红蛋白（HbAlc）、甘油三酯（TG）、低密度脂蛋白（LDL）、胆固醇（CHOL）、超氧化物歧化酶（SOD）活性、丙二醛（MDA）、超敏C反应蛋白（hs-CRP）、细胞黏附分子（ICAM-1）。结果 2组治疗后血清SOD活性均较治疗前明显增加,血清MDA含量均较治疗前明显降低。2组经α-硫辛酸或维生素C治疗后血清SOD活性均较治疗前明显增加,血清MDA含量均较治疗前、降糖治疗7d后明显降低。结论强化降糖治疗加用α-硫辛酸与维生素C存在一定抗氧化能力,但不能改善内皮细胞功能。     

硫辛酸注射液对糖尿病足患者氧化应激状态与局部微循环的影响

目的探讨硫辛酸注射液对糖尿病足患者氧化应激状态与局部微循环的影响。方法选取74例糖尿病足患者,随机分为2组。对照组进行常规的糖尿病足治疗,观察组则在对照组常规治疗的基础上加用硫辛酸注射液进行治疗。比较2组治疗前后的氧化应激状态与局部微循环指标。结果 2组治疗后的氧化应激状态与局部微循环指标均显著优于治疗前,且观察组显著优于对照组(P0.05)。结论硫辛酸注射液能改善糖尿病足患者的氧化应激状态与局部微循环状态。     

The involvement of endoplasmic reticulum stress in bile acid-induced hepatocellular injury

Secondary bile acids produced by enteric bacteria accumulate to high levels in the enterohepatic circulation and may contribute to the pathogenesis of hepatocellular injury. Relative hydrophobicity has been suggested to be an important determinant of the biological properties of these compounds, although the mechanism by which bile acids induce pathogenesis is not fully understood. On the other hand, endoplasmic reticulum stress has been shown to be involved in the induction and development of various pathogenic conditions. In this report, we demonstrated that the intensities of cytotoxicity and endoplasmic reticulum stress in HepG2 cells triggered by the bile acids tested were largely dependent on their hydrophobicity. The activation of caspase-3 and DNA fragmentation by treatment with chenodeoxycholic acid showed the contribution of apoptosis to cytotoxicity. Increases in intracellular calcium levels and the generation of reactive oxygen species stimulated by treatment with chenodeoxycholic acid contributed to endoplasmic reticulum stress. Bile acids also induced transforming growth factor-β, a potent profibrogenic factor, which is known to induce hepatocyte apoptosis and ultimately liver fibrosis. In conclusion, our study demonstrated that bile acids induced endoplasmic reticulum stress, which in turn stimulated apoptosis in HepG2 cells, in a hydrophobicity-dependent manner.     

Bile acid active and passive ileal transport in the rabbit: effect of luminal stirring

The intestinal absorption of bile acids (BA) with different chemical structure has been evaluated in the rabbit, after intestinal infusion of different concentrations (0.25-30 mM) of BA, by mesenteric blood sampling. Cholic (CA), chenodeoxycholic (CDCA), ursodeoxycholic (UDCA) acid, free and taurine (T-) conjugated, together with glycocholic (GCA) acid and deoxycholic acid (DCA) were studied. The apparent uptake parameters were calculated. All conjugated BA showed active transport (T max, nmol min-1 cm-1 int.), with Tmax values in the following order: TCA > TUDCA > TCDCA; unconjugated BA showed passive uptake, with values in the following order: DCA > CDCA > UDCA > CA. GCA and CA showed both passive uptake and active transport. For all BA studied the % uptake in the ileal segment considered was less than 10%, BA uptake being thus limited by transport and/or diffusion kinetics, rather than by flow velocity. The liquid resistance to BA radial diffusion inside the lumen was evaluated, and the infusate-to-blood uptake parameters corrected for it, in order to get the uptake parameters from the epithelium-to-liquid interface to mesenteric blood: the apparent Km decreased, passive uptake coefficient increased, while Tmax was unchanged. The passive component of the uptake, corrected for the luminal resistance, correlated with the BA hydrophobicity (r = 0.963; P < 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)     

肺结核患儿血清对氧磷酶活性与氧化应激指标的改变及其临床意义

目的探讨肺结核患儿血清对氧磷酶(PON1)活性与氧化应激指标的改变及其临床意义。方法连续性随机选取本院收治的肺结核患儿80例,综合分析患儿血清总氧化态(TOS)、总抗氧化态(TAS)和氧化应激指数(OSI)等氧化应激指标与PON1水平的改变及其相关性。结果肺结核患儿TAS明显低于对照组[(1.8±1.1)、(2.3±1.9)μmoL Trolox Eq/L,P0.05],而TOS和OSI明显高于对照组[(25.9±18.4)、(9.8±5.6)μmoL H2O2Eq/L,(13.3±7.7)、(4.5±2.1),P0.05]。在血清PON1水平方面,肺结核组明显低于对照组[(16.9±12.1)、(25.5±14.3)U/L,P0.05]。通过Pearson和Sperman相关性分析可见,PON1与TAS呈正相关(r=0.303,P0.05),与TOS和OSI呈负相关(rTOS=-0.283,rOSI=-0.228,P0.05)。结论肺结核患儿体内处于高氧化应激状态,同时PON1水平明显下降。     

Effect of ellagic acid on cyclosporine A-induced oxidative damage in the liver of rats

Cyclosporine A (CsA) is an immunosuppressor, which is most frequently used in the transplant surgery and in the treatment of autoimmune diseases. It has been shown that CsA is able to generate reactive oxygen species and lipid peroxidation, which are directly involved in the CsA nephrotoxicity, hepatotoxicity and cardiotoxicity. This study was undertaken to investigate the protective effect of ellagic acid (EA), a polyphenolic compound against CsA-induced liver injury in male Wistar rats. In this study, CsA was administered orally (25 mg/kg body weight) for 21 days to induce toxicity. EA was administered orally (12.5, 25 and 50 mg/kg body weight) for 21 days along with oral administration of CsA. CsA-induced liver damage was evidenced by increased activities of serum hepatic enzymes namely aspartate transaminase, alanine transaminase, alkaline phosphatase and lactate dehydrogenase with a significant elevation of lipid peroxidation markers such as thiobarbituric acid reactive substances (TBARS) and hydroperoxides in the liver. The levels of enzymic antioxidants such as superoxide dismutase, catalase and glutathione-S-transferase and non-enzymic antioxidants (vitamin C, vitamin E and reduced glutathione) were also decreased in CsA-treated rats. Administrations of EA at 50 mg/kg body weight significantly decreased the activities of hepatic marker enzymes compared with other doses of EA (12.5, 25 mg/kg body weight). In addition, the levels of TBARS and hydroperoxides were significantly decreased and the levels of enzymic and non-enzymic antioxidants significant increased on treatment with EA in the liver. The biochemical observation was supplemented by histopathologic examination of liver section. The results of this study indicate that EA might play an important role in protecting CsA-induced oxidative damage in the liver.     

便秘型肠易激综合征患者的血浆5-HT水平与氧化应激作用的相关性分析

目的分析便秘型肠易激综合征患者的血浆5-羟色胺(5-HT)表达与氧化应激作用的相关性。方法选择78例便秘型肠易激综合征患者作为观察组,78例健康人作为对照组,两组均进行血浆5-HT、脂质过氧化物(LPO)和丙二醛(MDA)的检测,以及空腹血糖(FBG)、血清总胆固醇(TC)、三酰甘油(TG)、低密度脂蛋白胆固醇(LDL-C)、高密度脂蛋白胆固醇(HDL-C)的检测与相关性分析。结果观察组的血浆MDA浓度(4.46±0.51)nmol/L高于对照组(1.68±0.38)nmol/L,差异有统计学意义(P0.05);观察组LPO浓度(18.67±1.48)nmol/L高于对照组(6.62±1.29)nmol/L,差异有统计学意义(P0.05)。观察组血浆5-HT浓度(1 828.44±300.87)pg/mL高于对照组(1 236.93±289.48)pg/mL,差异有统计学意义(P0.05)。偏相关分析便秘型肠易激综合征的血浆5-HT与MDA(r=0.325,P0.05)、LPO(r=0.432,P0.05)、TC(r=0.357,P0.05)都呈正相关,而与HDL-C(r=-0.385,P0.05)呈负相关;多因素Logistic回归分析显示MDA、LPO、TC与HDL-C都为影响5-HT的独立危险因素(P0.05)。结论便秘型肠易激综合征患者中血浆5-HT呈现高表达状况,同时伴随有MDA与LPO的高表达,且MDA与LPO的表达情况会影响5-HT的表达,可能是便秘型肠易激综合征的病理生理机制之一。