The research analyzed the expression and difference of MSTN/Smad signal path genes(MSTN, Smad2, Smad3,Smad4, TGFBR1, TGFBR2) in Turpan black sheep muscle tissue, as well as the correlation with some growth indices. Be...The research analyzed the expression and difference of MSTN/Smad signal path genes(MSTN, Smad2, Smad3,Smad4, TGFBR1, TGFBR2) in Turpan black sheep muscle tissue, as well as the correlation with some growth indices. Besides,the research used the fluorescence quantitative PCR technique to detect the expression level of MSTN, Smad2, Smad3, Smad4,TGFBR1 and TGFBR2 genes in m RNA of Turpan black sheep muscle. The research also used conventional and histological methods to determine the muscle growth and meat producibility indices, discussed the relationship between MSTN/Smad signal path and muscle growth and meat production. The result shows that these genes are expressed in Turpan black sheep muscle tissues, and have some relationship with body weight, height, length, chest circumference, hoof circumference, carcass and dressing percentage. The MSTN gene is negatively correlated with body weight(r = 0.993, P < 0.05), and hoof circumference(r= 0.957, p < 0.01), but has no significant correlation with body height, length, carcass weight, dressing percentages(P > 0.05);Smad2 gene shows significantly negative correlation the with dressing percentage(r = 0.918, p < 0.05), but no significant correlation with body weight, height, length, chest circumference, hoof circumference and carcass(P > 0.05); Smad3 gene shows no significant correlation with any of them(P > 0.05); Smad4, TGFBR1, TGFBR2 did not show any significant relationship with body height, length, chest circumference, weight and dressing percentage(P > 0.05).展开更多
AIM： To explore the role of transforming growth factorbeta1 （TGF-β1）-smad signal transduction pathway in patients with hepatocellular carcinoma. METHODS： Thirty-six hepatocellular carcinoma specimens were obtaine...AIM： To explore the role of transforming growth factorbeta1 （TGF-β1）-smad signal transduction pathway in patients with hepatocellular carcinoma. METHODS： Thirty-six hepatocellular carcinoma specimens were obtained from Qidong Liver Cancer Institute and Department of Pathology of the Second Affiliated Hospital of Nanjing Medical University. All primary antibodies （polyclonal antibodies） to TGF-β1, type H Transforming growth factor-beta receptor （TβR-Ⅱ）, nuclear factor-kappaB （NF-KB）, CD34, smad4 and smad7, secondary antibodies and immunohistochemical kit were purchased from Zhongshan Biotechnology Limited Company （Beijing, China）. The expressions of TGF-β1, TβR-Ⅱ, NF- KB, smad4 and smad7 proteins in 36 specimens of hepatocellular carcinoma （HCC） and its adjacent tissue were separately detected by immunohistochemistry to observe the relationship between TGF-β1 and TβR-Ⅱ, between NF-KB and TGF-β1, between smad4 and smad7 and between TGF-β1 or TβR-Ⅱ and microvessel density （MVD）. MVD was determined by labelling the vessel endothelial cells with CD34. RESULTS： The expression of TGF-β1, smad7 and MVD was higher in HCC tissue than in adjacent HCC tissue （P〈0.01, P〈0.05,P〈0.01 respectively）. The expression of TβR-Ⅱ and smad4 was lower in HCC tissue than in its adjacent tissue （P〈0.01, P〈0.05 respectively）. The expression of TGF-β1 protein and NF-KB protein was consistent in HCC tissue. The expression of TGF-β1 and MVD was also consistent in HCC tissue. The expression of TIER- Ⅱ was negatively correlated with that of MVD in HCC tissue. CONCLUSION： The expressions of TGF-IB1, TβR- Ⅱ, NF-KB, smad4 and smad7 in HCC tissue, which are major up and down stream factors of TGF-β1-smad signal transduction pathway, are abnormal. These factors are closely related with NVD and may play an important role in HCC angiogenesis. The inhibitory action of TGF-β1 is weakened in hepatic carcinoma cells because of abnormality of TGF-β1 receptors （such as TIBR- Ⅱ） and postreceptors （such as smad4 and smad7）. NF-KB may cause activation and production of TGF-β1.展开更多
Background: To explore the effects of electroacupuncture on cardiac function and myocardial fibrosis in rat models of heart failure, and to elucidate the underlying mechanism of electroacupuncture in heart failure tre...Background: To explore the effects of electroacupuncture on cardiac function and myocardial fibrosis in rat models of heart failure, and to elucidate the underlying mechanism of electroacupuncture in heart failure treatment. Methods: Healthy male Sprague-Dawley rats were allocated into three groups: Sham group, Model group, and electroacupuncture (Model + EA) group, with each group comprising 8 rats. The model underwent a procedure involving the ligation of the left anterior descending coronary artery to induce a model of heart failure. The Model + EA group was used for 7 consecutive days for electroacupuncture of bilateral Shenmen (HT7) and Tongli (HT5), once a day for 30 min each time. Left ventricular parameters in rats were assessed using a small-animal ultrasound machine to analyze changes in left ventricular end-diastolic volume, left ventricular end-systolic volume, left ventricular ejection fraction, and left ventricular fractional shortening. Serum interleukin-1β (IL-1β), cardiac troponin (cTn), and N-terminal brain natriuretic peptide precursor levels were measured using ELISA. Histopathological changes in rat myocardium were observed through HE staining, while collagen deposition in rat myocardial tissue was assessed using the Masson staining method. Picro sirius red staining, immunohistochemical staining, and RT-qPCR were utilized to distinguish between the various types of collagen deposition. The expression level of TGF-β1 and SMAD2/3/4/7 mRNA in rat myocardial tissues was determined using RT-qPCR. Additionally, western blot analysis was conducted to assess the protein expression levels of TGF-β1, SMAD3/7, and p-SMAD3 in rat myocardial tissues. Results: Compared with the Sham group, the left ventricular ejection fraction and left ventricular fractional shortening values of the Model group were significantly decreased (P < 0.01);the left ventricular end-diastolic volume and left ventricular end-systolic volume values were remarkably increased (P < 0.01);serum N-terminal brain natriuretic peptide precursor content was increased (P < 0.01);serum IL-1β and cTn levels were increased (P < 0.01);myocardial collagen volume fraction were increased (P < 0.01);and those of the expression of TGF-β1 and SMAD2/3/4 mRNA was increased (P < 0.01);the expression of SMAD7 mRNA was decreased (P < 0.01);the protein expression levels of TGF-β1, SMAD3, and p-Smad3 were increased (P < 0.01);the protein expression level of SMAD7 was decreased (P < 0.01) in the Model group. Compared to the Model group, the expression levels of the proteins TGF-β1, SMAD3, and p-Smad3 in myocardial tissue were found to be decreased (P < 0.01), and the expression level of the protein SMAD7 was found to be increased (P < 0.01) in the Model + EA group;the collagen volume fraction and deposition of type Ⅰ /Ⅲ collagen were decreased (P < 0.01) in the Model + EA group. Conclusion: Electroacupuncture alleviates myocardial fibrosis in rats with heart failure, and this effect is likely due to attributed to the modulation of the TGF-β1/Smads signaling pathway, which helps reduce collagen deposition in the extracellular matrix.展开更多
Background Hepatic fibrosis is the key stage of the pathological progress from hepatic injury to cirrhosis. Ursodeoxycholic acid （UDCA） has been known as having significant clinical therapeutic effects on chronic li...Background Hepatic fibrosis is the key stage of the pathological progress from hepatic injury to cirrhosis. Ursodeoxycholic acid （UDCA） has been known as having significant clinical therapeutic effects on chronic liver diseases. Our research aimed to study the effect of UDCA on the signaling pathway of transforming growth factor beta1 （TGFβ1）/Smad and discuss its possible molecular mechanisms of inhibiting hepatic fibrosis. Methods Rat hepatic stellate cells were cultured in vitro and randomly assigned to 4 groups. Group A was control group with only DMEM culture medium applied, and groups B, C, D were experimental groups, with different doses of UDCA （1.0 mmol/L, 0.5 mmol/L and 0.25 mmol/L respectively） added into their DMEM culture medium for further culture of 24 hours and 48 hours. The protein expressions of TGFβ1, TGF type 1 receptor, Smad3, Smad4 and Smad7 were measured by Western blotting, as well as the expressions of TGFβ1, Smad3, Smad7 and cAMP response element （CREB） binding protein （CBP） mRNA by real-time PCR. SPSS 11.5 statistical package was adopted for data analyses. Results Compared with control group, the mRNA expressions of TGFβ1 in the high and middle UDCA dose groups for 24 hours and 48 hours significantly decreased （P 〈0.05）, the protein expressions of TGFβ1 in the two above groups for 48 hours and in the high dose group for 24 hours significantly decreased （P 〈0.05）. The protein and mRNA expressions of Smad3 in each UDCA dose group for 24 hours and 48 hours significantly decreased, with significant difference among different UDCA dose groups and between that of 24 hours and 48 hours observed （P 〈0.05）. The protein and mRNA expressions of Smad7 in the high and middle UDCA dose groups for 24 hours and 48 hours significantly increased. The CBP mRNA expression in each UDCA dose group for 24 hours and 48 hours significantly decreased （P 〈0.05）, with significant difference among different UDCA dose groups observed （P 〈0.05）. Conclusion UDCA could curb the development of hepatic fibrosis through affecting the signaling pathway of TGFβ1/Smad by inhibiting the expressions of TGFβ1, Smad3 and CBP and increasing the expression of Smad7.展开更多
激素性股骨头坏死(steroid-induced osteonecrosis of the femoral head,SIONFH)是由于糖皮质激素使用不当或过度而引起的髋关节疾病,发病机制尚未统一,临床疗效亦不佳。当前,没有效果明确的药物可以延缓疾病进程,而中医药治疗SIONFH在...激素性股骨头坏死(steroid-induced osteonecrosis of the femoral head,SIONFH)是由于糖皮质激素使用不当或过度而引起的髋关节疾病,发病机制尚未统一,临床疗效亦不佳。当前,没有效果明确的药物可以延缓疾病进程,而中医药治疗SIONFH在临床上取得一定疗效。即便如此,仍未能完整的从分子生物及细胞生物学角度阐明中药治疗SIONFH的作用机制。转化生长因子-β(TGF-β)/骨形态发生蛋白(BMP)/Smad信号通路的转导是防治SIONFH的研究热点之一,故该文阐明了该信号通路的转导机制以及与SIONFH的联系,检索了基于该通路治疗SIONFH的全部中药及复方并阐述其影响机制。基于中医对SIONFH的认识,现临床上使用补肝肾强筋骨以及活血祛瘀通络类的方药治疗SIONFH,且具有良好的疗效。中药通过调控该通路,可刺激骨髓间充质干细胞成骨分化,降低破骨细胞含量,减少脂肪生成,改善微循环,抗氧化损伤,促进股骨头内血管新生,从而促进股骨头损伤的修复。现基于TGF-β/BMP/Smad信号通路对中医药治疗SIONFH的研究进展做一综述,期许为中医药治疗SIONFH提供理论依据及参考。展开更多
目的:研究祛瘀护膜法对反流性食管炎(RE)大鼠食管TGF-β/Smad通路及E-钙黏蛋白(E-Cadherin)表达的影响。方法:使用“4.2 mm幽门夹+2/3胃底结扎术”建立RE大鼠模型56只,造模成功后,随机分为西药组1、西药组2、治疗组、优化组、祛瘀护膜...目的:研究祛瘀护膜法对反流性食管炎(RE)大鼠食管TGF-β/Smad通路及E-钙黏蛋白(E-Cadherin)表达的影响。方法:使用“4.2 mm幽门夹+2/3胃底结扎术”建立RE大鼠模型56只,造模成功后,随机分为西药组1、西药组2、治疗组、优化组、祛瘀护膜剂组、加味祛瘀护膜剂组,每组8只,另设空白组8只。连续给药14 d,第15天采血后处死大鼠并取出食管组织。采用HE染色光镜下观察食管组织病理变化;透射电镜观察食管上皮细胞间隙;ELISA法检测转化生长因子-β1(TGF-β1)、肿瘤坏死因子-α(TNF-α)水平;RT-PCR法检测Snail m RNA、Slug m RNA、Twist m RNA、E-Cadherin m RNA表达水平;Western blotting检测TGF-β1、Snail、Slug、Twist、NLRP3、Smad2/3、p-Smad2/3蛋白表达水平;免疫组织化学染色测定TGF-β1、E-Cadherin、NLRP3表达。结果:祛瘀护膜法治疗的RE大鼠一般情况好转,体质量增加;食管黏膜损伤改善;上皮细胞间隙呈缩小趋势;食管组织中TGF-β1、Snail、Slug、Twist、NLRP3蛋白表达及Smad2/3磷酸化占比低于模型组(P<0.05),E-Cadherin蛋白及E-Cadherin m RNA表达高于模型组(P<0.05);血清中TNF-α、TGF-β1低于模型组(P<0.05)。结论:祛瘀护膜法可能通过抑制TGF-β/Smad信号通路,干预该通路介导的E-cadherin表达,促进食管炎黏膜修复,拮抗RE大鼠食管黏膜炎症。展开更多
文摘The research analyzed the expression and difference of MSTN/Smad signal path genes(MSTN, Smad2, Smad3,Smad4, TGFBR1, TGFBR2) in Turpan black sheep muscle tissue, as well as the correlation with some growth indices. Besides,the research used the fluorescence quantitative PCR technique to detect the expression level of MSTN, Smad2, Smad3, Smad4,TGFBR1 and TGFBR2 genes in m RNA of Turpan black sheep muscle. The research also used conventional and histological methods to determine the muscle growth and meat producibility indices, discussed the relationship between MSTN/Smad signal path and muscle growth and meat production. The result shows that these genes are expressed in Turpan black sheep muscle tissues, and have some relationship with body weight, height, length, chest circumference, hoof circumference, carcass and dressing percentage. The MSTN gene is negatively correlated with body weight(r = 0.993, P < 0.05), and hoof circumference(r= 0.957, p < 0.01), but has no significant correlation with body height, length, carcass weight, dressing percentages(P > 0.05);Smad2 gene shows significantly negative correlation the with dressing percentage(r = 0.918, p < 0.05), but no significant correlation with body weight, height, length, chest circumference, hoof circumference and carcass(P > 0.05); Smad3 gene shows no significant correlation with any of them(P > 0.05); Smad4, TGFBR1, TGFBR2 did not show any significant relationship with body height, length, chest circumference, weight and dressing percentage(P > 0.05).
基金Supported by Natural Science Foundation of Jiangsu Province, No. BK2001168 Natural Science Foundation of Department of Education of Jiangsu Province, No. 02KJD320023 Science and Technology Innovation Foundation of Nanjing Medical University, No. CX2004004.
文摘AIM： To explore the role of transforming growth factorbeta1 （TGF-β1）-smad signal transduction pathway in patients with hepatocellular carcinoma. METHODS： Thirty-six hepatocellular carcinoma specimens were obtained from Qidong Liver Cancer Institute and Department of Pathology of the Second Affiliated Hospital of Nanjing Medical University. All primary antibodies （polyclonal antibodies） to TGF-β1, type H Transforming growth factor-beta receptor （TβR-Ⅱ）, nuclear factor-kappaB （NF-KB）, CD34, smad4 and smad7, secondary antibodies and immunohistochemical kit were purchased from Zhongshan Biotechnology Limited Company （Beijing, China）. The expressions of TGF-β1, TβR-Ⅱ, NF- KB, smad4 and smad7 proteins in 36 specimens of hepatocellular carcinoma （HCC） and its adjacent tissue were separately detected by immunohistochemistry to observe the relationship between TGF-β1 and TβR-Ⅱ, between NF-KB and TGF-β1, between smad4 and smad7 and between TGF-β1 or TβR-Ⅱ and microvessel density （MVD）. MVD was determined by labelling the vessel endothelial cells with CD34. RESULTS： The expression of TGF-β1, smad7 and MVD was higher in HCC tissue than in adjacent HCC tissue （P〈0.01, P〈0.05,P〈0.01 respectively）. The expression of TβR-Ⅱ and smad4 was lower in HCC tissue than in its adjacent tissue （P〈0.01, P〈0.05 respectively）. The expression of TGF-β1 protein and NF-KB protein was consistent in HCC tissue. The expression of TGF-β1 and MVD was also consistent in HCC tissue. The expression of TIER- Ⅱ was negatively correlated with that of MVD in HCC tissue. CONCLUSION： The expressions of TGF-IB1, TβR- Ⅱ, NF-KB, smad4 and smad7 in HCC tissue, which are major up and down stream factors of TGF-β1-smad signal transduction pathway, are abnormal. These factors are closely related with NVD and may play an important role in HCC angiogenesis. The inhibitory action of TGF-β1 is weakened in hepatic carcinoma cells because of abnormality of TGF-β1 receptors （such as TIBR- Ⅱ） and postreceptors （such as smad4 and smad7）. NF-KB may cause activation and production of TGF-β1.
基金the China’s National Key Research and Development Program Projects(No.2022YFC3500500 and No.2022YFC3500502).
文摘Background: To explore the effects of electroacupuncture on cardiac function and myocardial fibrosis in rat models of heart failure, and to elucidate the underlying mechanism of electroacupuncture in heart failure treatment. Methods: Healthy male Sprague-Dawley rats were allocated into three groups: Sham group, Model group, and electroacupuncture (Model + EA) group, with each group comprising 8 rats. The model underwent a procedure involving the ligation of the left anterior descending coronary artery to induce a model of heart failure. The Model + EA group was used for 7 consecutive days for electroacupuncture of bilateral Shenmen (HT7) and Tongli (HT5), once a day for 30 min each time. Left ventricular parameters in rats were assessed using a small-animal ultrasound machine to analyze changes in left ventricular end-diastolic volume, left ventricular end-systolic volume, left ventricular ejection fraction, and left ventricular fractional shortening. Serum interleukin-1β (IL-1β), cardiac troponin (cTn), and N-terminal brain natriuretic peptide precursor levels were measured using ELISA. Histopathological changes in rat myocardium were observed through HE staining, while collagen deposition in rat myocardial tissue was assessed using the Masson staining method. Picro sirius red staining, immunohistochemical staining, and RT-qPCR were utilized to distinguish between the various types of collagen deposition. The expression level of TGF-β1 and SMAD2/3/4/7 mRNA in rat myocardial tissues was determined using RT-qPCR. Additionally, western blot analysis was conducted to assess the protein expression levels of TGF-β1, SMAD3/7, and p-SMAD3 in rat myocardial tissues. Results: Compared with the Sham group, the left ventricular ejection fraction and left ventricular fractional shortening values of the Model group were significantly decreased (P < 0.01);the left ventricular end-diastolic volume and left ventricular end-systolic volume values were remarkably increased (P < 0.01);serum N-terminal brain natriuretic peptide precursor content was increased (P < 0.01);serum IL-1β and cTn levels were increased (P < 0.01);myocardial collagen volume fraction were increased (P < 0.01);and those of the expression of TGF-β1 and SMAD2/3/4 mRNA was increased (P < 0.01);the expression of SMAD7 mRNA was decreased (P < 0.01);the protein expression levels of TGF-β1, SMAD3, and p-Smad3 were increased (P < 0.01);the protein expression level of SMAD7 was decreased (P < 0.01) in the Model group. Compared to the Model group, the expression levels of the proteins TGF-β1, SMAD3, and p-Smad3 in myocardial tissue were found to be decreased (P < 0.01), and the expression level of the protein SMAD7 was found to be increased (P < 0.01) in the Model + EA group;the collagen volume fraction and deposition of type Ⅰ /Ⅲ collagen were decreased (P < 0.01) in the Model + EA group. Conclusion: Electroacupuncture alleviates myocardial fibrosis in rats with heart failure, and this effect is likely due to attributed to the modulation of the TGF-β1/Smads signaling pathway, which helps reduce collagen deposition in the extracellular matrix.
文摘Background Hepatic fibrosis is the key stage of the pathological progress from hepatic injury to cirrhosis. Ursodeoxycholic acid （UDCA） has been known as having significant clinical therapeutic effects on chronic liver diseases. Our research aimed to study the effect of UDCA on the signaling pathway of transforming growth factor beta1 （TGFβ1）/Smad and discuss its possible molecular mechanisms of inhibiting hepatic fibrosis. Methods Rat hepatic stellate cells were cultured in vitro and randomly assigned to 4 groups. Group A was control group with only DMEM culture medium applied, and groups B, C, D were experimental groups, with different doses of UDCA （1.0 mmol/L, 0.5 mmol/L and 0.25 mmol/L respectively） added into their DMEM culture medium for further culture of 24 hours and 48 hours. The protein expressions of TGFβ1, TGF type 1 receptor, Smad3, Smad4 and Smad7 were measured by Western blotting, as well as the expressions of TGFβ1, Smad3, Smad7 and cAMP response element （CREB） binding protein （CBP） mRNA by real-time PCR. SPSS 11.5 statistical package was adopted for data analyses. Results Compared with control group, the mRNA expressions of TGFβ1 in the high and middle UDCA dose groups for 24 hours and 48 hours significantly decreased （P 〈0.05）, the protein expressions of TGFβ1 in the two above groups for 48 hours and in the high dose group for 24 hours significantly decreased （P 〈0.05）. The protein and mRNA expressions of Smad3 in each UDCA dose group for 24 hours and 48 hours significantly decreased, with significant difference among different UDCA dose groups and between that of 24 hours and 48 hours observed （P 〈0.05）. The protein and mRNA expressions of Smad7 in the high and middle UDCA dose groups for 24 hours and 48 hours significantly increased. The CBP mRNA expression in each UDCA dose group for 24 hours and 48 hours significantly decreased （P 〈0.05）, with significant difference among different UDCA dose groups observed （P 〈0.05）. Conclusion UDCA could curb the development of hepatic fibrosis through affecting the signaling pathway of TGFβ1/Smad by inhibiting the expressions of TGFβ1, Smad3 and CBP and increasing the expression of Smad7.
文摘激素性股骨头坏死(steroid-induced osteonecrosis of the femoral head,SIONFH)是由于糖皮质激素使用不当或过度而引起的髋关节疾病,发病机制尚未统一,临床疗效亦不佳。当前,没有效果明确的药物可以延缓疾病进程,而中医药治疗SIONFH在临床上取得一定疗效。即便如此,仍未能完整的从分子生物及细胞生物学角度阐明中药治疗SIONFH的作用机制。转化生长因子-β(TGF-β)/骨形态发生蛋白(BMP)/Smad信号通路的转导是防治SIONFH的研究热点之一,故该文阐明了该信号通路的转导机制以及与SIONFH的联系,检索了基于该通路治疗SIONFH的全部中药及复方并阐述其影响机制。基于中医对SIONFH的认识,现临床上使用补肝肾强筋骨以及活血祛瘀通络类的方药治疗SIONFH,且具有良好的疗效。中药通过调控该通路,可刺激骨髓间充质干细胞成骨分化,降低破骨细胞含量,减少脂肪生成,改善微循环,抗氧化损伤,促进股骨头内血管新生,从而促进股骨头损伤的修复。现基于TGF-β/BMP/Smad信号通路对中医药治疗SIONFH的研究进展做一综述,期许为中医药治疗SIONFH提供理论依据及参考。
文摘目的:研究祛瘀护膜法对反流性食管炎(RE)大鼠食管TGF-β/Smad通路及E-钙黏蛋白(E-Cadherin)表达的影响。方法:使用“4.2 mm幽门夹+2/3胃底结扎术”建立RE大鼠模型56只,造模成功后,随机分为西药组1、西药组2、治疗组、优化组、祛瘀护膜剂组、加味祛瘀护膜剂组,每组8只,另设空白组8只。连续给药14 d,第15天采血后处死大鼠并取出食管组织。采用HE染色光镜下观察食管组织病理变化;透射电镜观察食管上皮细胞间隙;ELISA法检测转化生长因子-β1(TGF-β1)、肿瘤坏死因子-α(TNF-α)水平;RT-PCR法检测Snail m RNA、Slug m RNA、Twist m RNA、E-Cadherin m RNA表达水平;Western blotting检测TGF-β1、Snail、Slug、Twist、NLRP3、Smad2/3、p-Smad2/3蛋白表达水平;免疫组织化学染色测定TGF-β1、E-Cadherin、NLRP3表达。结果:祛瘀护膜法治疗的RE大鼠一般情况好转,体质量增加;食管黏膜损伤改善;上皮细胞间隙呈缩小趋势;食管组织中TGF-β1、Snail、Slug、Twist、NLRP3蛋白表达及Smad2/3磷酸化占比低于模型组(P<0.05),E-Cadherin蛋白及E-Cadherin m RNA表达高于模型组(P<0.05);血清中TNF-α、TGF-β1低于模型组(P<0.05)。结论:祛瘀护膜法可能通过抑制TGF-β/Smad信号通路,干预该通路介导的E-cadherin表达,促进食管炎黏膜修复,拮抗RE大鼠食管黏膜炎症。
