Objective:Diabetic kidney disease (DKD) is one of the most serious complications of type 2 diabetes mellitus (T2DM), and bone metabolism disorders show a close linkage to DKD. Thus, this study aimed to explore the association between bone turnover markers (BTMs) and DKD. Methods:In present cross-sectional study, serum BTMs were detected in 1433 hospitalized patients with T2DM. Logistic regression analysis was used to investigate the associations between osteocalcin (N-MID), β-cross-linked C-telopeptide (β-CTX), total type I collagen N-terminal propeptide (PINP), and the risk of DKD. Results:The circulation N-MID, β-CTX, and PINP levels were significantly lower in the DKD group compared with the non-DKD group (all P < 0.05), especially in male and aged < 60 subgroups. Serum BTM levels showed a weak correlations with certain glucose metabolism parameters-such as glycated hemoglobin, fasting blood glucose, C peptide, and fasting insulin-as well as alkaline phosphatase (ALP) levels and low-density lipoprotein (all P < 0.001). A weak negative correlation was also observed with the duration of diabetes (all P < 0.0001). In addition, β-CTX levels showed a minimal positive correlation with eGFR (r = 0.057, P=0.036) and a modest correlation with ALP (r = 0.31, P < 0.0001). After adjusting for potential confounders, higher serum β-CTX levels were independently associated with a lower risk of DKD. However, no significant associations were found among serum N-MID, PINP, and the risk of DKD. Conclusion:BTM levels were significantly decreased in patients with DKD. Lower β-CTX levels were independently associated with a larger prevalence of DKD after adjusting for potential confounders, suggesting that serum β-CTX may be an independent marker associated with the risk of DKD.

ABSTRACT The immune response to Mycoplasma pneumoniae infection plays a key role in clinical symptoms. Previous investigations focused on the pro-inflammatory effects of leukocytes and the pivotal role of epithelial cell metabolic status in finely modulating the inflammatory response have been neglected. Herein, we examined how glycolysis in airway epithelial cells is affected by M. pneumoniae infection in an in vitro model. Additionally, we investigated the contribution of ATP to pulmonary inflammation. Metabolic analysis revealed a marked metabolic shift in bronchial epithelial cells during M. pneumoniae infection, characterized by increased glucose uptake, enhanced aerobic glycolysis, and augmented ATP synthesis. Notably, these metabolic alterations are orchestrated by adaptor proteins, MyD88 and TRAM. The resulting synthesized ATP is released into the extracellular milieu via vesicular exocytosis and pannexin protein channels, leading to a substantial increase in extracellular ATP levels. The conditioned medium supernatant from M. pneumoniae -infected epithelial cells enhances the secretion of both interleukin (IL)-1β and IL-18 by peripheral blood mononuclear cells, partially mediated by the P2X7 purine receptor (P2X7R). In vivo experiments confirm that addition of a conditioned medium exacerbates pulmonary inflammation, which can be attenuated by pre-treatment with a P2X7R inhibitor. Collectively, these findings highlight the significance of airway epithelial aerobic glycolysis in enhancing the pulmonary inflammatory response and aiding pathogen clearance.

Neutrophils are essential cells involved in inflammation. However, the specific mechanism of neutrophil chemotaxis induced by Treponema pallidum remains unknown. In this study, human umbilical vein endothelial cells (HUVECs) were utilized as target cells to investigate the expression levels of chemokines when stimulated with different concentrations of Tp0768 (also known as TpN44.5 or TmpA, a T. pallidum infection dependent antigen). The results indicated that Tp0768 treatment enhanced neutrophil chemotaxis in HUVECs, which was closely associated with the expression levels of CXCL1, CXCL2, and CXCL8 (also known as interleukin-8). At the same time, the results show that the Toll-like receptor 2 (TLR2) signaling pathway is activated and that endoplasmic reticulum (ER) stress occurs. Furthermore, the findings revealed that the use of protein kinase RNA-like endoplasmic reticulum kinase (PERK) and immunoglobulin-regulated enhancer 1 (IRE1) inhibitors reduced the expression levels of CXCL1, CXCL2, and CXCL8. Additionally, inhibiting TLR2 significantly decreased the expression levels of ER stress-related proteins (PERK and IRE1), CXCL1, CXCL2, and CXCL8. Consequently, neutrophil chemotaxis was significantly inhibited after treatment with TLR2, PERK, and IRE1 inhibitors. These findings shed light on the role of Tp0768 in enhancing neutrophil chemotaxis in endothelial cells, providing a foundation for further exploration of syphilis pathogenesis and offering a new direction for the diagnosis and treatment of T. pallidum infection.

目的 初步比较2种新冠核酸检测试剂盒的灵敏度和精密度,评估两种试剂盒在新冠肺炎核酸检测能力的优劣,为新冠病毒核酸检测试剂的选择提供一定的参考.方法 选择新冠肺炎确诊病例咽拭子样本55个,非新冠患者咽拭子样本28例,用两种试剂盒进行检测,分析其一致性;将新冠肺炎确诊病例的咽拭子样本进行10×梯度稀释及倍比稀释,分别用两种试剂盒检测,比较分析其灵敏度;用两种试剂分别检测不同浓度的样本,比较两种试剂盒的精密度.结果(1)试剂A、B的检出率分别为100％、98.2％,符合度分别为98.8％、98.8％,Kappa值分别为0.973、0.964;试剂A、B的双靶标(ORF1ab基因和N基因)阳性率分别为90.7％、79.6％,单靶标(ORF1ab基因或N基因)阳性率分别为9.3％、20.4％.(2)试剂B可稳定检测到100×稀释的样本,而试剂A可以稳定检测到1000×稀释的样本;样本经800×稀释后,试剂A、B的检出率分别是100％、62.5％;样本经1000×稀释后试剂A、B的检出率分别是100％、25％.(3)样本原液经2种试剂检测后,试剂A的N基因及ORF1ab基因的CV％值分别为2.1、2.1,试剂B的N基因及ORF1ab基因的CV％值分别为0.8、1.0,经统计分析两者之间精密度,差异无统计学意义(P<0.05);样本经10×稀释后,试剂A与B的N基因CV％值分别为0.7、2.1(F=8.31,P<0.05),ORF1ab基因CV％值分别为0.6、2.3(F=15.614,P<0.05);样本经100×稀释后,试剂A与B的N基因CV％值分别为3.1、8.9(F=5.684,P<0.05),ORF1ab基因CV％值分别为1.9、6.0(F=5.846,P<0.05);样本经10倍梯度稀释后试剂B的N基因CV％分别为0.8、2.1、8.9,ORF1ab基因CV％分别为1.0、2.3、6.0,精密度随着样本浓度降低而降低.结论 试剂A灵敏度高、重复性好、符合度高,复检率相对较低,整体检测效果A>B.

Objective To study the difference of MICA allele distribution in Jingzhou and Hengyang.Methods The sample MICA allele was detected by PCR-SSP and PCR-SBT.Results Eight MICA alleles were detected in Hengyang group and Jingzhou group,MICA*027 was not detected in Hengyang group,MICA*009N in Jingzhou group,the three alleles in Jingzhou patient group were MICA*00201 and MICA*019 and MICA*and the 3 alleles in Hengyang patient group were MICA*010,MICA*00201 and MICA*01201 and MICA alleles between the two groups.The MICA allele type,MICA-STR allele distribu-tion frequency and MICA-STR allele type detected in Hengyang group and Jingzhou group were all different,but the overall dis-tribution was not significantly different(P＞0.05).Conclusion MICA allele frequency distribution varies between lung cancer pop-ulation of Hunan and Hubei.

Selenium (Se) remains to have an inconsistent relationship with glycemic biomarkers and the risk of developing type 2 diabetes (T2D). Few studies have investigated the relationship between blood Se and glycemic biomarkers among people with normoglycemia. We conducted a cross-sectional analysis using the U.S. National Health and Nutrition Examination Survey 2013–2016. Multivariable linear regression models were developed to examine the associations of blood Se with glycemic biomarkers, namely, fasting plasma glucose (FPG), hemoglobin A1c (HbA1c), insulin, and the oral glucose tolerance test (OGTT). Blood Se was treated as continuous (per log-10 increment) and categorical exposure (in quartiles) in separate regression models. We assessed the dose–response relationships by restricted cubic spline analysis. After excluding the participants with T2D or incomplete data, 2706 participants were analyzed. The highest quartile of blood Se was associated with increased FPG [adjusted β = 0.12, 95% Confidence Intervals (CI) = 0.04, 0.20], OGTT (adjusted β = 0.29, 95% CI = 0.02, 0.56), HbA1c (adjusted β = 0.04, 95% CI = 0.00, 0.07), and insulin (adjusted β = 2.50, 95% CI = 1.05, 3.95) compared with the lowest quartile. Positive associations were also observed between every log-10 increment of blood Se level and glycemic biomarkers, except for OGTT. A positive linear dose–response relationship existed between blood Se and FPG (Poverall = 0.003, Pnonlinear = 0.073) and insulin (Poverall = 0.004, Pnonlinear =0.060). BMI, age, and smoking status modified the associations of the highest quartile of Se (compared with the lowest quartile) with glycemic biomarkers. Overall, positive associations of blood Se with glycemic biomarkers were observed among U.S. adults with normoglycemia. These findings implied that people with normoglycemia need to be aware of the level of Se and other mineral intakes from diet and supplements. Further research is required to identify the mechanisms of excess Se in the progression of diabetes.

Background Syphilis is a chronic sexually transmitted disease caused by Treponema pallidum subspecies pallidum ( T. pallidum ), which is a public health problem that seriously affects human health worldwide. T. pallidum is characterized by early transmission and immune escape and is therefore termed an “invisible pathogen”. Methods This review systematically summarizes the host’s innate and adaptive immune responses to T. pallidum infection as well as the escape mechanisms of T. pallidum . Purpose To lay the foundation for assessing the pathogenic mechanism and the systematic prevention and treatment of syphilis. Conclusion The immune escape mechanism of T. pallidum plays an important role in its survival. Exploring the occurrence and development of these mechanisms has laid the foundation for the development of syphilis vaccine.

目的 原核表达沙眼衣原体(Chlamydia trachomatis,Ct)CT622蛋白,制备CT622多克隆抗体,初步探讨CT622蛋白对HeLa细胞增殖的影响,为进一步阐明CT622蛋白在沙眼衣原体致病中的作用提供实验依据.方法 以Ct D型基因组为模板构建原核表达重组载体pGEX-6p-1/CT622;重组载体经IPTG诱导表达,Glutathione Sepharose 4B beads纯化GST-CT622融合蛋白,PreScission Protease酶切除GST标签后获取纯化的CT622蛋白;将纯化的CT622蛋白去内毒素处理后,经皮下免疫新西兰兔获取抗CT622抗体,采用抗原亲和纯化层析柱进行抗体纯化,BCA测定抗体浓度,SDS-PAGE鉴定多克隆抗体纯度,ELISA检测抗体效价;用不同浓度的CT622蛋白处理HeLa细胞24 h,CCK-8细胞活性检测试剂盒检测细胞存活率(％).结果 成功表达并纯化了 CT622蛋白,该蛋白最佳表达条件为IPTG终浓度0.8 mol/L,30℃、180 r/min条件下诱导4 h.制备兔源性抗CT622多克隆抗体,纯化后抗CT622抗体浓度为0.75 mg/ml,纯度＞70％,ELISA检测免疫兔血清抗体效价为1 ∶ 512 000左右;经1～15 μg/ml浓度梯度的CT622蛋白处理HeLa细胞后,其细胞存活率高于对照组.结论 成功表达、纯化了沙眼衣原体CT622蛋白,制备了高效价兔源性抗CT622抗体.在一定浓度范围内,CT622蛋白能促进HeLa细胞的增殖.

Abstract Background Lipid and glucose metabolism abnormalities are associated with nonalcoholic fatty liver disease (NAFLD). The triglyceride–glucose (TyG) index is a recently developed indicator that can identify individuals at risk for NAFLD. However, the applicability of the TyG index for identifying NAFLD in patients with type 2 diabetes mellitus (T2DM) is unclear. The aim of this study was to investigate the ability of the TyG index to identify individuals at risk for NAFLD in the T2DM population. Methods A total of 2280 participants with T2DM were recruited in this cross-sectional study. The TyG index was calculated, and NAFLD was diagnosed by ultrasonography. Binary logistic regression models were used to evaluate the association of the TyG index, glycemic parameters and lipid parameters with NAFLD. Results Logistic regression analysis showed that the TyG index was significantly associated with NAFLD in subjects with T2DM, the odds ratio (OR) were 3.27 (95% confidence interval [CI], 2.03–5.27; P < 0.001) for NAFLD in the highest TyG quartile after adjustment for known confounders. In stratified analysis, an elevated TyG index were more remarkably associated with NAFLD in younger patients (< 65 years; OR, 2.35; 95% CI, 1.83–3.02; P < 0.001), females (OR, 2.69; 95% CI, 1.67–4.32; P < 0.001), patients with BMI < 25 kg/m2 (OR, 2.80; 95% CI, 2.01–3.91; P < 0.0001), and with lower high-density lipoprotein cholesterol (< 1 mmol/L; OR, 2.76; 95% CI, 1.98–3.83; P < 0.001). Conclusion The TyG index is significantly associated with NAFLD and shows superior ability for identify NAFLD risk compared with other lipid and glycemic parameters in T2DM.

Endoplasmic reticulum (ER) stress and oxidative stress (OS) are often related states in cells as part of normal physiology but more frequently manifested in the pathophysiology of many diseases, particularly diseases involving acute or chronic inflammation. In this study, we reviewed recent findings about the role of ER stress and OS in the pathogenesis of inflammatory diseases.

Endothelial microparticles (EMPs) can be released in chronic kidney disease (CKD). Plasma concentration of high inorganic phosphate (HP) is considered as a decisive determinant of vascular calcification in CKD. We therefore explored the role of HP-induced EMPs (HP-EMPs) in the vascular calcification and its potential mechanism. We observed the shape of HP-EMPs captured by vascular smooth muscle cells (VSMCs) dynamically changed from rare dots, rosettes, to semicircle or circle. Our results demonstrated that HP-EMPs could directly promote VSMC calcification, or accelerate HP-induced calcification through signal transducers and activators of transcription 3 (STAT3)/bone morphogenetic protein-2 (BMP2) signaling pathway. AEG-1 activity was increased through HP-EMPs-induced VSMC calcification, in arteries from uremic rats, or from uremic rats treated with HP-EMPs. AEG-1 deficiency blocked, whereas AEG-1 overexpression exacerbated, the calcium deposition of VSMCs. AEG-1, a target of miR-153-3p, could be suppressed by agomiR-153-3p. Notably, VSMC-specific enhance of miR-153-3p by tail vein injection of aptamer-agomiR-153-3p decreased calcium deposition in both uremia rats treated with HP-EMPs or not. HP-EMPs could directly induce VSMCs calcification and accelerate Pi-induced calcification, and AEG-1 may act as crucial regulator of HP-EMPs-induced vascular calcification. This study sheds light on the therapeutic agents that influence HP-EMPs production or AEG-1 activity, which may be of benefit to treat vascular calcification.

Objective This study aimed to investigate the association of serum bone turnover markers (BTMs) with metabolic syndrome components and carotid atherosclerosis in patients with type 2 diabetes mellitus (T2DM). Methods We performed a cross-sectional based study in T2DM populations. Serum BTMs including N-terminal osteocalcin (N-MID), β-cross-linked C-telopeptide of type I collagen (β-CTX), and procollagen type I N-terminal propeptide (PINP) were measured by immunoassay method. Carotid artery intima-media thickness and carotid artery plaque (CAP) were measured by B-mode ultrasound. Results The serum N-MID, PINP, and β-CTX levels significantly lower in the CAP group compared with the non-CAP group. N-MID and PINP levels were inversely associated with fasting blood glucose, HOMA-IR, CRP, eGFR, and triglycerides (all P < 0.05), whereas β-CTX levels were negatively associated with triglycerides (P < 0.05). After multiple adjustment, the odds ratios (ORs) were substantially higher for CAP with decreased N-MID level (OR = 0.958; 95% CI = 0.926–0.991; P = 0.013). However, serum levels of PINP and β-CTX were not associated with the presence of CAP. Multivariate logistic regression analysis further revealed that serum N-MID, PINP, and β-CTX levels were significantly associated with hypertriglyceridemia, whereas serum N-MID and β-CTX levels were associated with overweight/obesity risk. Conclusions These findings indicated that serum N-MID level was an independent risk factor for carotid atherosclerosis, whereas BTM levels were associated with other metabolic syndrome components in a T2DM population.

研究MICA等位基因多态性与海南人群HBV感染易感性之间的关联性.采用PCR-SSP和PCR-SBT方法对样本MICA等位基因的多态性进行检测.HBV感染患者中共检出10种MICA等位基因和5种MICA-STR等位基因,和对照组相比较,MICA010、MICA-A5等位基因可能对HBV感染易感(MICA010:OR=3.88,95％CI:2.19～6.85,P=0.000;MICA-A5:OR=1.27,95％CI:0.92～1.77,P=0.0068).MICA008/045基因型可能对HBV感染不易感,MICA010/010纯合子基因型可能对HBV易感(MICA 008/045:OR=0.09,95％CI:0.01～1.74,P=0.0071;MICA010/010:OR=4.41,95％CI:1.26～15.46,P=0.0106).MICA等位基因多态性与海南人群HBV感染的易感性间存在关联性.

The disease progression and morbidity of tuberculosis (TB) infections are determined by virulence of the microorganism, host genetic factors and environmental factors. The highly polymorphic MHC class I chain-related gene (MIC) could serve as a potential host genetic candidate. To investigate the association of MIC polymorphism with TB infection, 124 patients and 191 ethnically matched controls from Hunan province, Southern China, were genotyped for the MIC polymorphism using polymerase chain reaction-sequence specific priming and sequencing-based typing. The results showed that allele frequencies of MIC-sequence and MICA-STR were different in TB patients in comparison to normal controls (both P < 0.05). MICA-A4 and MICA*012:01 alleles were positive associated (OR = 2.42, 95% CI: 1.69-3.87; OR = 3.41, 95% CI: 2.19-5.33, respectively, both P-c < 0.05) while MICA -A5 were inversely associated (OR = 0.59, 95%CI: 0.41-0.94, P-c < 0.05) with TB. Homozygote MICA*012:01/012:01 was observed to have significant risk effects on TB (OR = 4.76, 95% CI: 1.94-11.69, P(c)0000-0001-5151-1853 < 0.05). Additionally, MICB*008 allele conduct a significant risk effect for TB (OR = 3.17, 95%CI: 1.80-5.61, P-c < 0.05). All the data showed that MIC polymorphism was associated with the variable susceptibility to TB in Chinese population.

Objective:To investigate the association between MIC allele polymorphism and susceptibility to Ureaplasma urealyticum infection. Methods:PCR-SSP and PCR-SBT were used to analyze the gene polymorphism of every one. Results:Twelve allele genes of MICA and five MICA-STR and fourteen MICB were found in the participants,the frequency of MICA?010 and MICB?009N were higher in ureaplasma urealyticum infection patients than in healthy controls(MICA?010:OR=3. 85,95%CI:2. 12-6. 99, Pc<0. 05;MICB?009N:OR=3. 22,95%CI:1. 33-7. 80,Pc<0. 05);the frequencies of MICA-A5. 1 and MICB?00502 were lower in ureaplasma urealyticum infection patients than in healthy controls(MICA-A5. 1:OR=0. 61,95%CI:0. 40-0. 94,Pc<0. 05;MICB?00502:OR=0. 58,95%CI:0. 40-0. 83,Pc<0. 05),the differences were statistically significant;MICA?010/010,MICA?01201/01201 homozygote were higher in ureaplasma urealyticum infection patients than in healthy controls(MICA?010/010:OR=14. 84, 95%CI:1. 90-115. 9,Pc<0. 05:MICA?01201/01201:OR=10. 83,95%CI:1. 35-86. 79,Pc<0. 05),the differences were statistically significant. The distribution frequency of MICB?00502/00502 in patients with ureaplasma urealyticum was higher,but the difference was not statistically significant(Pc>0. 05). Conclusion:MIC allele gene polymorphism may be associated with ureaplasma urealyticum infection.

Objective To study the association between the MICA gene polymorphism and haplotype diversity with the susceptibility of ovarian cancer. Methods PCR-SSP and PCR-SBT were used to analyze the gene polymorphism and haplotype diversity of MICA in ovarian cancer patients and healthy individuals. Results Eleven MICA allele genes were found in the south China ovarian cancer patients, and the frequency of MICA * 010 was higher in south China ovarian cancer patients than in healthy controls, presenting genic susceptibility to ovarian cancer ( O^R = 6.43, 95% CI: 3.51, 11.76, < 0.05). Five MICA-STR alleles were detected, but there was no significant difference between the case and the control. Compared to the control group, the distribution frequency of MICA * 010/010 was significantly high and it is probably a susceptibility genotype to ovarian cancer ( O^R= 14.82, 95% CI: 1.89, 115.94, <0.05). Conclusions allele gene polymorphism and haplotype diversity may be associated with ovarian cancer.

Objective:To study the association MICB gene polymorphism and breast cancer in han nationality of Hain-an.Methods:PCR-SSP and PCR-SBT were used to analyze the gene polymorphism of MICB.Results:Forty allele genes were found in patients of breast cancer,The frequencies of MICB*002 and MICB*014 were lower in breast cancer pa-tients than in healthy controls,although the frequencies of MICB*016 and MICB*003 were higher;MICB*016 and MICB*003 allele genes may be susceptible to breast cancer (MICB *016:OR=10.68,95% CI:2.52-45.28,Pc<0.05;MICB*003:OR=3.57,95% CI:1.34-9.49,Pc<0.05),and MICB*002 and MICB*014 allele genes may-be protected(MICB*002:OR=0.31,95% CI:0.19-0.51,Pc<0.05;MICB*014:OR=0.32,95% CI:0.17-0.60,Pc<0.05);MICB* 002/002 and MICB*014/014 genotypes maybe protected to breast cancer (MICB*002/002:OR=0.12,95% CI:0.04-0.36,Pc<0.05;MICB*014/014:OR=0.30,95% CI:0.10-0.89,Pc<0.05).Conclu-sions:MICB allele gene polymorphism may be associated with breast cancer.

目的:研究海南汉族人群MICB等位基因的多态性与肺癌易感性之间的关联性.方法:采用PCR-SSP(PCR sequence-specific primers)和PCR-SBT(PCR sequence-based typing)方法对样本MICB等位基因的多态性进行检测.结果:肺癌患者中检出14种MICB等位基因;和对照组相比较,MICB*00502等位基因在肺癌患者组分布频率较少(43.5％ vs 57.8％),MICB * 016等位基因在肺癌患者组分布较多(5.9％vs 0.6％);MICB* 016等位基因可能对肺癌易感(OR=11.19,95％ CI:2.59-48.24,Pc ＜0.05);MICB* 00502等位基因可能对肺癌不易感(MICB* 00502:OR=0.56,95％ CI:0.42-0.76,Pc ＜0.05).结论:MICB等位基因的多态性与肺癌的易感性之间存在关联性.

Objective To compare the serum homocysteine (HCY) levels in patients with five types of malignant tumors. Methods A total of 153 cases of malignant tumors,including 31 with lung cancer,37 with colorectal cancer,33 with cervical can-cer,27 with primary hepatic carcinoma and 25 with breast cancer admitted into Jiangxi cancer hospital from October 2015 to Jan-uary 2016,were selected as the objects of study. The serum HCY levels were measured by circulating enzymeassay. Results ⑴There were significant differences in the serum HCY level among group A1,B1,C1,D1 and E1(P<0.05). The serum HCY levels in group A1 were significantly higher than that in group C1,D1 and E1,respectively (P<0.05),while statistical difference in serum HCY level were not present between any other 2 groups (P>0.05). There were no significant differences in serum HCY level among group A2,B2,C2,D2 and E2 (P>0.05). ⑵There were no significant differences in serum HCY level among group A3,B3,C3,D3 and E3 (P>0.05),and no statistical differences in serum HCY level among group A4,B4 and C4 (P>0.05). Conclusion There are differences in some degree in serum HCY level among 5 different types of malignant tumor,and the patients with primary hepatic carcinoma are more susceptible to hyperhomocysteine.

Objective:To investigate the expression of IL-6 and STAT3 in the epilepsy rat caused by penicillin .Methods:The model of epilepsy in rats was made by abdominal injecting penicillin .Then the EEG and behavior was observed in each group and the level of IL-6/STAT3 transcription and cytokine IL-6 secretion in different groups was compared using qRT-PCR and ELISA respectively.The protein expression of STAT3 was detected using Western blot.Results: 500 U/kg and 800 U/kg rats injected penicillin were induced epilepsy and show typical epileptic seizures behavioral and brain waves ,seizures was 100%;the level of IL-6/STAT3 transcription and IL-6 secretion in the model of epilepsy was significantly higher than control .There was no significant difference in the expression of STAT3 protein levels,but a significant increase in p-STAT3.Conclusion:Expression of STAT3 and IL-6 plays an important role in the Epilepsy Rat caused by penicillin .