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1.
Purpose The diaphragm is one of the organs directly affected by abdominal sepsis. Evidence suggests that sepsis induces diaphragmatic fatigability and that activated neutrophils play a crucial role in the development of diaphragmatic fatigability. In the present study, we investigated whether olprinone, a phosphodiesterase inhibitor, influenced the kinetics of cytokine-induced neutrophil chemoattractant-1 (CINC-1) in the diaphragm under abdominal septic conditions. Methods Male Wistar rats were randomly assigned to a sham group, a cecal ligation and perforation group, and a phosphodiesterase inhibitor-pretreated group. To measure serial changes in CINC-1 concentrations, the right hemidiaphragm was removed at 4, 8, and 16 h after the surgical procedure in each group. Result In the cecal ligation and perforation group, CINC-1 concentrations in the diaphragm were significantly elevated compared with those in the sham group at both 4 and 8 h after the cecal ligation and perforation procedure. In the phosphodiesterase inhibitor-pretreated group, olprinone significantly attenuated the elevated CINC-1 concentrations at both 4 and 8 h after the surgical procedure. However, we observed no statistically significant differences in CINC-1 concentrations between the cecal ligation and perforation group and the phosphodiesterase inhibitor-pretreated groups at 16 h after the surgical procedure. Conclusion Olprinone decreases elevated CINC-1 concentration in the diaphragm under septic conditions. This suggests that olprinone may inhibit neutrophil recruitment to the diaphragm.  相似文献   

2.
目的:探讨内毒素血症大鼠外周血中性粒细胞(PMN)表面CD11b表达与内毒素性肺损伤的关系。方法:大肠杆菌E-Coli O111B4 4mg/kg尾静脉注射制备大鼠内毒素血症动物模型。112只大鼠随机分为对照组(静脉注射等量生理盐水)及内毒素注射后1h组、2h组、4h组、8h组、12h组、24h组,每组16只动物。在相应时间点放血处死动物,分别取股静脉血、肺组织及进行支气管肺泡灌洗,测定肺组织湿/干重(W/D)比值、肺组织髓过氧化物酶(MPO)活性和支气管肺泡灌洗液(BALF)总蛋白定量等肺损伤指标。流式细胞仪测定外周血PMN表面CD11b表达。另取16只大鼠,内毒素注射后2h时测定外周血PMN表面CD11b表达,24h时放血处死,测定上述指标。结果:①大鼠内毒素血症可以造成明显的急性肺损伤,表现为肺组织W/D比值、MPO活性和BALF总蛋白明显增高,分别在2h、8h和2h显著高于对照组(P〈0.05或P〈0.01),峰值分别出现在内毒素注射后12h、24h和12h;②大鼠内毒素性肺损伤时,外周血PMN表面CD11b表达水平在早期(1h)明显升高(与对照组比较,P〈O.05),在2h达到峰值,之后逐渐降低;③外周血CD11b表达峰值明显早于肺组织W/D比、MPO和BALF总蛋白等肺损伤指标的峰值出现时间;④同一动物2h时外周血PMN表面CD11b的表达水平与其24h时肺组织W/D比、MPO和BALF总蛋白含量呈显著正相关(r分别为0.78、0.77和0.73,P〈0.05)。结论:内毒素性肺损伤中,外周血CD11b表达升高可能有助于内毒素性肺损伤的早期诊断,并可能预示以后的肺损伤程度。  相似文献   

3.
BACKGROUND: We have demonstrated that uraemic neutrophils that exhibit a low intracellular pH (pHi) display enhanced phagocytosis. However, the underlying cellular mechanism is unclear. METHODS: We used neutrophils from three groups of haemodialysis (HD) patients before dialysis (Groups A, B and C) and also from age- and sex-matched healthy individuals to determine pHi, phagocytosis and expression of CD11b, CD18, CD14 and toll-like receptors (TLR)-2 and TLR-4. The patients were categorized based on three consecutive monthly pre-dialysis plasma bicarbonate concentrations(P(HCO3)) and pH values; Groups A, B and C had a constant pre-dialysis P(HCO3) of /=26 mmol/L (mEq/L), respectively. We also studied the effects induced by the correction of metabolic acidosis and monoclonal antibodies (mAbs) against CD11b/CD18 on neutrophils in Group A. Furthermore, we investigated the effect of intracellular acidification on uraemic neutrophils ex vivo. RESULTS: We observed that the neutrophils in Group A exhibited significantly increased phagocytosis and expression of CD11b/CD18 compared with those in Groups B and C. Additionally, our ex vivo studies demonstrated that the mAbs against CD11b/CD18 partially blocked the enhancement of neutrophil phagocytosis in Group A. Moreover, the pHi of uraemic neutrophils is inversely correlated with phagocytosis and expression of CD11b/CD18. CONCLUSIONS: HD patients with a low P(HCO3) exhibited low neutrophil pHi that in turn increased the expression of CD11b/CD18 compared with neutrophils with a normal or high pHi. This increased expression of CD11b/CD18 on the uraemic neutrophils may contribute to the pHi-mediated phagocytosis.  相似文献   

4.
BACKGROUND: Acute lung injury (ALI) is a progressive syndrome associated with significant mortality in sepsis patients. Neutrophils are key cells in the inflammatory response that characterizes ALI. This study was designed to explore the effects of hydroxyethyl starch (HES) 130/0.4 (a novel plasma substitute) on pulmonary neutrophil recruitment and associated ALI in a rat sepsis model induced by cecal ligation and puncture (CLP). METHODS: Animals were randomly assigned to six groups [saline control; CLP and saline; CLP and HES (7.5, 15 and 30 ml/kg); and HES control], subjected to CLP and infused with or without HES 130/0.4 4 h after CLP. Six hours later, the pulmonary capillary permeability (PCP), myeloperoxidase (MPO) activity, lung histological changes, tumor necrosis factor-alpha, interleukin-1beta and cytokine-induced neutrophil chemoattractant levels, P-selectin mRNA expression and nuclear factor-kappa B (NF-kappaB) activation were measured. RESULTS: Resuscitation with HES 130/0.4 significantly attenuated the CLP-induced increase in PCP, MPO activity, cytokine/chemokine levels, mRNA expression of P-selectin and NF-kappaB activation, all of which are involved in the recruitment of neutrophils. Groups receiving the higher doses of HES 130/0.4 (15 and 30 ml/kg) were more adequately resuscitated. CONCLUSION: HES 130/0.4 can inhibit CLP-induced neutrophil recruitment and subsequent ALI by attenuating cytokines/chemokines, adhesion molecule-mediated inflammation and NF-kappaB activation.  相似文献   

5.
Introduction: Urine neutrophil gelatinase-associated lipocalin (uNGAL) is a rapidly emerging biomarker for early detection of acute kidney injury (AKI). We aimed to investigate the prevalence and prognostic value of the early uNGAL in patients with AKI induced by sepsis. Methods: In this prospective cohort study, we analyzed the case records of 126 septic patients with and without AKI and evaluated the uNGAL for early prediction and risk stratification of septic patients with AKI. Results: Of 126 patients analyzed, 58 (46%) developed septic AKI. Men comprised more than half (68%) of the sample population, the mean age (SD) was 57 years. The prognostic accuracy of uNGAL, as quantified by the area under the receiver-operating-characteristic curve (AU-ROC), was highest with peak uNGAL (AU-ROC: 0.86; 95% CI: 0.81–0.93), as compared with the admission uNGAL (AU-ROC: 0.81; 95% CI: 0.73–0.89). The peak uNGAL correlated with the levels of peak blood urea nitrogen (r?=?0.674) and serum creatinine (r?=?0.608), the length of hospital stay (r?=?0.602) and weakly correlated with the number of hemodialysis sessions that each patient received during hospital stay (r?=?0.405). By multivariate analysis, increased peak uNGAL remained independently associated with the development of septic AKI (odds ratio: 32.12; 95% CI: 6.21–90.37; p?Conclusions: uNGAL is independently associated with subsequent AKI among patients with sepsis.  相似文献   

6.
What’s known on the subject? and What does the study add? Following ischemic damage, reperfusion may cause further injury paradoxically in the ischemic tissue, known as reperfusion injury. Decreased blood flow causes hypoxia, leading to increased levels of lactic acid, hypoxanthine, and lipid peroxides in ischemic tissues and subsequent increase in blood flow after lipid peroxidation produces reactive oxygen species. In addition, several experimental studies and clinical trials demonstrated that unilateral testicular torsion has a detrimental effect also to the contralateral testis. Although the basic pathological mechanism underlying testicular ischemia/reperfusion injury has not been completely understood, it has been shown that reactive oxygen species formed during ischemia/reperfusion play the key role in this process. In the international literature there is no information available regarding the effects of neutrophil elastase inhibitors such as sivelestat sodium aminoacetate tetrahydrate on the ischemia/reperfusion injury of the testis. In this study we investigated the effects of sivelestat in the testes bilaterally, after unilateral testicular ischemia/reperfusion injury using an experimental unilateral testicular ischemia/reperfusion rat model. We found that sivelestat reduces the oxidative stress and partially prevents the testicular damage both in the ischemic and in the contralateral testis.

OBJECTIVE

To investigate the effect of a neutrophil elastase inhibitor, sivelestat sodium hydrate, on testicular ischaemia–reperfusion (IR)‐injury.

MATERIAL AND METHODS

Eight‐week‐old male Sprague–Dawley rats were divided into four groups: sham‐operated control rats; IR rats (group IR); and IR rats that received intra‐abdominal administration of 15 mg/kg or 60 mg/kg sivelestat (group IR15 and group IR60, respectively). Right testicular vessels were clamped for 90 min in groups IR, IR15 and IR60. Sivelestat had been administered 45 min after the induction of the ischaemia in groups IR15 and IR60. In subpopulations of IR, IR15 and IR60 rats, reperfusion was performed after ischaemia for 2 h (groups IR‐A, IR15‐A and IR60‐A, respectively) or 48 h (groups IR‐B, IR15‐B and IR60‐B, respectively). At the end of the reperfusion period, blood samples were aspirated from both spermatic veins of each rat and testosterone was evaluated. Then both testes from all rats were collected and tissue levels of malondialdehyde (MDA), myeloperoxidase (MPO), and heat‐shock protein‐70(HSP‐70) were evaluated. Testicular tissue samples were also processed for histological evaluation and TUNEL staining.

RESULTS

MDA, MPO and HSP‐70 levels in the ischemic testis were significantly higher in the IR group compared with the control group. MDA and HSP‐70 in the contralateral testis were significantly higher in the IR group compared with the control group. Bilateral testosterone levels were lower in all rat groups in comparison with the control group. Bilateral testicular samples in group IR showed extensive histopathologic degenerative alterations and increased percentage of apoptotic cells. Sivelestat treatment lowered the MDA concentration and the percentage of apoptotic cells bilaterally and ameliorated the testicular histological pattern bilaterally.

CONCLUSIONS

Unilateral testicular ischaemia causes significant contralateral testicular damage. Sivelestat may be a novel adjunct tool for reducing oxidative stress and partially preventing bilateral testicular damage.  相似文献   

7.

Background

Acid aspiration induces lung injury by causing an intense inflammatory reaction. Neutrophils are attracted by various cytokines, such as TNFβ, and release reactive oxygen species, which then cause acute lung injury. Endothelin antagonists, such as bosentan, have been found to possess anti-inflammatory properties.

Materials and methods

We performed a prospective, randomised, controlled study to evaluate the effects of bosentan in a rat model of acid-induced lung injury. Sprague-Dawley rats underwent sevoflurane anaesthesia; lung injury was then induced by instillation of 1.2 mL/kg, 0.1 M hydrochloric acid. The lungs were ventilated for 6 h and then randomised into three groups: bosentan 30 mg/kg body weight, 90 mg/kg body weight or sodium chloride, each applied immediately after acid aspiration via a gastric tube.

Results

After induction of acute lung inflammation, the production of reactive oxygen species by PMN following stimulation with FMLP increased significantly. Comparison of pre-treatment and post-treatment in the 90 mg/kg bosentan treatment group did not show a significant increase of reactive oxygen species following stimulation with FMLP. A comparison of the absolute difference of the MESF demonstrated a significant difference between the control group and the group treated with 90 mg/kg bosentan.

Conclusions

Bosentan administration at 90 mg/kg body weight reduced the release of reactive oxygen species after 360 min in acid aspiration-induced lung injury in rats.  相似文献   

8.
为探讨烧伤血清作用下 PMN-EC 粘附力的改变和 CD11/CD18单抗(mAb)对 PMN 与内皮细胞(EC)粘附力的影响,将烧伤血清与人 PMN 或人脐静脉内细胞(HUVEC)一同孵育,在孵育1,3,6,12,24小时分别应用细胞微管吸吮技术系统测定 PMN-HUVEC 粘附力,并用健康人血清刺激作对照。同时,将与烧伤血清孵育1,6,24小时的 PMN,应用 CD11a/CD18mAb 和 CD11b/CD18mAb 处理后,再测其与HUVEC 粘附力。结果表明:PMN 在烧伤血清刺激后与正常 HUVEC 粘附力迅速升高,1小时达到最高峰,并在24小时内维持此水平。烧伤血清激活的 PMN 与 HUVEC 粘附力可被 CD11a/CD18单抗和CD11b/CD18单抗降低70%~80%。HUVEC 在烧伤血清刺激后与 PMN 粘附力呈持续升高趋势,12小时后达最大值,并在以后12小时内无明显变化。提示:烧伤血清具有促进 PMN-EC 粘附,并在烧伤后PMN-EC 粘附中起重要作用,而且刺激 PMN 后所引起的 PMN-EC 粘附力变化与刺激 EC 后所引起的变化不同。CD11/CD18可部分降低 PMN-EC 粘附力,从而可能减轻 PMN 对 EC 的损害。  相似文献   

9.
Combined growth hormone (GH) and insulin-like growth factor-I (IGF-I) therapy has been advocated for clinical use to minimize the diabetogenic effect of GH and enhance their anabolic effects. However, GH has been shown to accelerate the development of glomerular sclerosis in experimental animals and IGF-I mediates the renal effects of GH. The purpose of this study was therefore to examine morphometrically the effects of GH (1 mg intraperitoneally three times a week), IGF-I (50 g/kg body weight subcutaneously twice a day), and combined GH/IGF-I treatments in vivo on mesangial matrix at 3–20 days after 5/6 nephrectomy in 140- to 150-g rats. There were no significant changes in growth and renal function after GH and/or IGF-I treatment. The effects of GH and IGF-I on glomerular size were additive, which were more prominent in juxtamedullary glomeruli. GH induced proportional increases in mesangial area (MA) and glomerular area (GA), whereas IGF-I induced a similar increase in GA without a corresponding change in MA. When compared with GH treatment alone, combined GH/IGF-I treatment resulted in a lesser degree of mesangial expansion despite an enhanced glomerular size. While additional studies are needed to examine the long-term effects of these findings, our results suggest a potentially beneficial effect of combined GH/IGF-I therapy during uremia.  相似文献   

10.
11.
目的 探讨大鼠内毒素性急性肺损伤(acute lung injury,ALI)时应用丙泊酚后处理对肺组织磷酸化c-Jun氨基末端激酶(phospho-c-Jun terninal kinnase,p-JNK)的影响.方法 96只雄性SD大鼠按数字随机表法分为4组(每组24只):生理盐水对照组(A组);内毒素[有效成分为...  相似文献   

12.
电刺激迷走神经对感染性休克大鼠急性肺损伤的影响   总被引:3,自引:3,他引:0  
目的 观察通过电刺激迷走神经研究胆碱能抗炎通路对感染性休克大鼠急性肺损伤的保护作用。方法 成年雄性SD大鼠40只,随机分为4组:假CLP组(SHAM)、CLP组(CLP)、迷走神经切断组(VGX)、迷走神经电刺激组(STM),每组10只,均采用盲肠结扎穿孔法(CLP)复制感染性休克模型,VGX组CLP后行双侧颈部迷走神经离断术,STM组在CLP基础上将左迷走神经远端连接刺激电极,于CLP术毕即刻予以持续电刺激(5V、2ms和1Hz)20min。动物均连续监测平均动脉压(MAP),分别在各组模型制备完毕或电刺激后0、1、2和4h检测血浆肿瘤坏死因子(TNF)-α含量、4h抽动脉血行血气分析计算呼吸指数和取肺组织观察肺组织病理学变化。结果 CLP组和VGX组MAP进行性下降,STM组血压各时间点均显著高于CLP组相应值。STM组血浆TNFα含量显著低于CLP组和VGX组。4hCLP组和VGX组pH值、PaO2、PaCO2和PaO2/FiO2显著下降(P〈0.01),明显低于假CLP组和STM组(P〈0.05)。光镜下CLP组和VGX组肺组织损害明显重于STM组和SHAM组。结论 电刺激迷走神经通过胆碱能抗炎通路能逆转CLP致感染性休克大鼠血压下降,降低血清TNFα水平,减轻急性肺损伤所致低氧血症和肺水肿,减轻肺组织病理损害,对肺脏有保护作用。  相似文献   

13.
目的研究丙酮酸乙酯对脓毒症肺损伤大鼠细胞间粘附分子1(ICAM1)的影响,探讨丙酮酸乙酯保护大鼠脓毒症肺损伤的作用机制。方法采用盲肠结扎穿孔术复制脓毒症肺损伤动物模型,30只Wistar大鼠随机分为假手术组、脓毒症肺损伤组和丙酮酸乙酯(40mg/kg,腹腔内注射)治疗组,每组10只。所有大鼠12h后活杀,用免疫组织化学方法检测肺组织中ICAM1的分布和表达,用免疫印迹法检测肺组织ICAM1蛋白水平的表达,检测支气管肺泡灌洗液白细胞计数、肺湿/干重比和肺组织髓过氧化物酶(MPOase)活性。结果与脓毒症肺损伤组比较,丙酮酸乙酯治疗组免疫印迹法和免疫组织化学法显示肺组织ICAM1的表达显著降低,肺泡灌洗液白细胞计数、肺湿/干重比和MPOase活性降低(P<0.01)。结论丙酮酸乙酯通过抑制肺组织ICAM1的表达,对脓毒症肺损伤大鼠具有保护作用。  相似文献   

14.
Background Our study evaluated the influence of short-term growth hormone treatment on the remnant kidney in 5/6 nephrectomized uremic rats Methods Twenty male Sprague-Dawley rats were divided into 4 groups: sham-operated control rats (SC, n=4); sham-operated rats treated with recombinant human growth hormone (SGH, n=4); uremic (5/6 nephrectomized) control rats (UrC, n=6); and uremic rats treated with recombinant human growth hormone (UrGH, n=6). Total food intake, food efficiency, average daily food intake per 100 g body weight, weight gain, increase in body length, creatinine clearance, and kidney weight per 100 g body weight were measured. Glomerular tuft area was determined, and the severity of glomerular sclerosis was scored. Insulin-like growth factor-I was localized in the kidneys by immunostaining. Results Weight gain, increase in body length, food efficiency, and food intake per unit body weight were greatest in the SGH group; in UrGH animals, food efficiency and food intake per unit body weight were significantly higher than those in UrC rats. Creatinine clearance in uremic rats was significantly reduced compared with that in sham-operated animals. There was no difference in the ratio of kidney weight to body weight among the groups. The average glomerular area was greatest, and the glomerular sclerosis index was highest, in the UrGH group. No insulin-like growth factor-I could be identified in the glomeruli. Conclusions Growth-hormone treatment augmented daily food intake, and the more rapid progression to glomerular sclerosis in hormone-treated uremic rats is probably due mainly to increased daily protein intake. This study was partly presented at both the 38th Annual Meeting of the Japanese Society of Nephrology and the Sixth Asian Pacific Congress of Nephrology  相似文献   

15.
Previous studies have suggested that insulin-like growth factor-I (IGF-I) and its binding proteins (IGFBPs) have a pathogenetic role in idiopathic osteoporosis. To investigate this question further we compared 20 men with idiopathic osteoporosis with 12 healthy, age-matched men regarding growth hormone (GH) secretion and sensitivity. GH samples were drawn every 30 minutes for 24 hours from 12 of the patients and all controls, and cumulated GH secretion (24hGH) was derived. Peak GH secretion (peakGH) was provoked by an insulin tolerance test. There were no differences between the groups in serum IGF-I (162 ± 30 vs 163 ± 47 μg/liter, mean ± SD), IGFBP-3 (2474 ± 263 vs 2568 ± 197 μg/liter), 24hGH (1.34 ± 1.26 vs 0.79 ± 0.43 U), or peakGH (53.0 ± 21.5 vs 44.1 ± 19.8 mU/liter). Patients and controls were given GH (2.4 U/day) for 1 week. Serum levels of markers for bone turnover increased significantly in both groups, with no difference in response to GH between the groups. The increase in urinary bone resorption markers was only significant in the controls. In the patients, but not in the controls, there were significant positive correlations between indices for GH secretion and markers for bone turnover at baseline and significant negative correlations with relative changes in bone markers during GH treatment. In this study no difference in GH secretion was found between men with idiopathic osteoporosis and controls, but the findings suggest that the GH/IGF-I axis could play a regulatory role in bone metabolism in men with this condition.  相似文献   

16.
Resveratrol reduces renal and lung injury caused by sepsis in rats   总被引:7,自引:0,他引:7  
Resveratrol (3,5,4'-trans-trihydroxystilbene), a natural phytoalexin, has various pharmacological effects, including anti-inflammatory properties via inhibition of oxidation, leukocyte priming, and expression of inflammatory mediators. The present study was aimed to investigate the possible beneficial activities of resveratrol on lung and kidney damage in a rat model of sepsis. MATERIALS AND METHODS: Sepsis was induced to Sprague-Dawley rats of both sexes (200-250 g) by cecal ligation and perforation. The rats were treated with resveratrol (30 mg/kg; i.p.) or saline after induction of sepsis and at 16 h. Twenty-four hours after the sepsis-induction, all rats were decapitated. Blood was collected for the measurement of tumor necrosis factor-alpha level and lactate dehydrogenase activity. Lung and kidney samples were taken for histological assessment and for the measurement of malondialdehyde, glutathione level, myeloperoxidase activity, and collagen content. RESULTS: Sepsis caused a significant increase in malondialdehyde levels, myeloperoxidase activity, and collagen content of the lung and kidney tissues with a concomitant reduction in glutathione levels. Microscopic examination revealed severe destruction of regular morphology in both lung and kidney tissues. Serum tumor necrosis factor-alpha and lactate dehydrogenase levels also were higher in rats with sepsis compared to those of the sham group. Resveratrol treatment reversed these biochemical parameters and preserved tissue morphology as evidenced by histological evaluation. CONCLUSIONS: Resveratrol, a phenolic compound, reduces sepsis-induced remote organ injury, at least in part, through its ability to balance oxidant-antioxidant status, to inhibit neutrophil infiltration and to regulate the release of inflammatory mediators.  相似文献   

17.
18.
BACKGROUND: We sought to investigate the potential therapeutic effects of acupuncture stimulation of ST-36 (Zusanli) on endotoxemia-induced acute lung injury in lipopolysaccharide (LPS)-stimulated rats. METHODS: Sixty rats were randomized into six groups (n = 10): (i) lipopolysaccharide (LPS) control group, (ii) normal saline (N/S) control group, (iii) LPS plus ST-36 group, (iv) N/S plus ST-36 group, (v) LPS plus sham point (Sham) group, and (vi) N/S plus Sham group. Manual acupuncture stimulation of ST-36 (designated as 'ST-36') or a 'non-acupoint' (designated as 'Sham') was performed in lightly immobilized rats for 30 min. Then, LPS injection was employed to induce sepsis. Rats were killed at 6 h after LPS injection and lung injury, nitric oxide (NO) biosynthesis and inducible NO synthase (iNOS) expression were assayed. RESULTS: Significant lung injury, pulmonary iNOS expression and systemic and pulmonary NO biosynthesis were noted in the LPS groups. Rats in the LPS plus Sham group had lung injury, pulmonary iNOS expression, systemic and pulmonary NO biosynthesis similar to those observed in the LPS group. However, the degree of lung injury, pulmonary iNOS expression and pulmonary NO biosynthesis, but not systemic NO biosynthesis, were significantly attenuated in the LPS plus ST-36 group as compared with those in both the LPS group and the LPS plus Sham group. CONCLUSION: Acupuncture stimulation of ST-36 may be effective as a prophylaxis measure against sepsis. However, results from this study do not support the use of acupuncture for the treatment of sepsis.  相似文献   

19.
目的:探讨改进型实验性左侧精索静脉曲张(ELV)对大鼠血清卵泡刺激素(FSH)及抑制素B(InhB)的影响。方法:利用改进的方法建立青春期SD大鼠左精索静脉曲张的模型30只;假手术组SD大鼠30只作对照组。术后3个月,取大鼠血清,ELISA法分别检测FSH、InhB的浓度。结果:实验组大鼠血清中FSH浓度[(37.56±9.72)ng/ml]与对照组[(26.69±5.33)ng/ml]相比升高,具有统计学意义(P<0.05);而实验组大鼠血清中InhB的浓度[(349.93±99.48)pg/ml]与对照组[(768.83±146.96)pg/ml]相比下降,具有统计学意义(P<0.05)。结论:改进型ELV致FSH升高及InhB下降,这些变化可能是影响生育能力的机制之一。  相似文献   

20.
目的 探讨重组人促红细胞生成素(rHuEP())对大鼠脊髓损伤后中性粒细胞趋化因子(CINC-1)表达的影响。方法 SD大鼠102只,随机分为4组,采用改良Allen’s脊髓损伤打击模型,以逆转录一聚合酶链反应(RT-PCR)法测定伤段脊髓组织CINC-1mRNA的表达情况。结果 正常脊髓组织内存在CINC-1mRNA的表达,脊髓损伤后CINC-1mRNA表达迅速增高,伤后6h达到高峰;rHuEPO治疗组脊髓损伤后6、12小时CINC-1mRNA表达明显低于NS治疗组.结论 CINC-1参与继发性脊髓损伤过程,rHuEPO抑制脊髓损伤后CINC-1mRNA的表达,对脊髓继发性损伤可能有保护作用,、  相似文献   

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