本文關(guān)鍵詞：慢性淺表性胃炎脾虛證患者與健康人物質(zhì)能量代謝基因差異表達(dá)研究，由筆耕文化傳播整理發(fā)布。

楊澤民,王穎芳,陳蔚文.慢性淺表性胃炎脾虛證患者與健康人物質(zhì)能量代謝基因差異表達(dá)研究[J].,2013,33(2):159-163

慢性淺表性胃炎脾虛證患者與健康人物質(zhì)能量代謝基因差異表達(dá)研究

Research on Differentially Expressed Genes Related to Substance and Energy Metabolism between Healthy Volunteers and Splenasthenic Syndrome Patients with Chronic Superficial Gastritis

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DOI：

中文關(guān)鍵詞:  脾虛證  DNA芯片  物質(zhì)代謝  慢性淺表性胃炎

英文關(guān)鍵詞:splenasthenic syndrome  DNA microarray  substance metabolism  chronic superficial gastritis

基金項(xiàng)目:國(guó)家自然科學(xué)基金重大研究計(jì)劃重點(diǎn)項(xiàng)目（ No. 90209004 ）；廣東省自然科學(xué)基金重點(diǎn)項(xiàng)目（ No. 05102323）；上海市教育委員會(huì)E－研究院建設(shè)計(jì)劃項(xiàng)目（No. E03008）； 國(guó)家自然科學(xué)基金青年基金資助項(xiàng)目（No. 81102703）

作者單位E-mail

楊澤民，王穎芳   

陳蔚文 廣州中醫(yī)藥大學(xué)脾胃研究所（廣州510405）；上海市高校中醫(yī)內(nèi)科學(xué)E－研究院，上海中醫(yī)藥大學(xué)（上海201203 ）； chenww@gzhtcm.edu.cn 

摘要點(diǎn)擊次數(shù): 703

全文下載次數(shù): 264

中文摘要:

      目的 分析慢性淺表性胃炎脾虛證患者體內(nèi)脂類(lèi)、蛋白質(zhì)、糖類(lèi)和核酸代謝情況，從物質(zhì)能量代謝的角度探討脾虛證的病理發(fā)生機(jī)制。方法 選擇4例2004年6月—2005年3月就診于廣州中醫(yī)藥大學(xué)一附院和廣東省中醫(yī)院的慢性淺表性胃炎脾虛證患者，選擇廣州中醫(yī)藥大學(xué)健康人4名，鉗取患者及健康人胃黏膜進(jìn)行DNA芯片實(shí)驗(yàn)，利用BRB ArrayTools和IPA軟件對(duì)DNA芯片雙通道數(shù)據(jù)進(jìn)行數(shù)據(jù)挖掘和生物信息學(xué)分析。結(jié)果 獲得15個(gè)與物質(zhì)能量代謝相關(guān)差異基因，占總差異表達(dá)基因（20個(gè)）的75%，其中上調(diào)基因1個(gè)，下調(diào)基因14個(gè)，11個(gè)基因?yàn)槊富�。其中脂�?lèi)代謝相關(guān)差異基因有ACAA2和CYP20A1，表現(xiàn)為脂肪酸分解和膽固醇轉(zhuǎn)化降低；蛋白質(zhì)代謝相關(guān)差異基因有ALDH9A1、ASL、ASS1、PCYOX1L、RPS28、UBE2D2、UBXN1、B3GNT1、GCNT1和PPP1R3C，表現(xiàn)為影響自主神經(jīng)、尿素循環(huán)等生物學(xué)過(guò)程的氨基酸代謝降低，蛋白質(zhì)合成降低，錯(cuò)誤折疊蛋白泛素化降解增加，翻譯后糖基化和磷酸化修飾降低；糖類(lèi)代謝相關(guān)差異基因有PPP1R3C、B3GNT1和GCNT1，表現(xiàn)為糖原和聚糖合成降低；核酸代謝相關(guān)差異基因有RMI1、SMARCD3和 PARP1，表現(xiàn)為DNA復(fù)制和轉(zhuǎn)錄降低，DNA損傷修復(fù)增加。結(jié)論 慢性淺表性胃炎脾虛證患者體內(nèi)脂類(lèi)、蛋白質(zhì)、糖類(lèi)和核酸代謝水平明顯降低，并且主要表現(xiàn)為酶基因表達(dá)下調(diào)，推測(cè)此可能是導(dǎo)致脾虛證營(yíng)養(yǎng)代謝障礙的重要機(jī)制之一。

英文摘要:

      Objective To analyze the metabolic states of the lipids， protein， carbohydrate， and nucleic acid for chronic superficial gastritis patients of splenasthenic syndrome （SS）， and to explore the pathogenesis mechanism of SS based on substance and energy metabolisms. Methods During June 2004 to March 2005， recruited were four chronic superficial gastritis patients of SS who visited at the First Hospital of Guangzhou University of Chinese Medicine and Guangdong Provincial Hospital of Traditional Chinese Medicine. Four healthy volunteers were recruited from Guangzhou University of Chinese Medicine. Their gastric mucosa was extracted to perform experiments of DNA microarray. The dual channel DNA microarray data were mined and bioinformatically analyzed by BRB ArrayTools and IPA software. Results Fifteen genes were involved in substance and energy metabolisms in 20 differentially expressed genes， accounting for 75%. Among these genes， one gene was up regulated， 14 genes down regulated， and 11 genes were enzyme gene. Differentially expressed genes related to lipid metabolism included ACAA2 and CYP20A1， manifested as fatty acid catabolism and cholesterol transformation. Genes related to protein metabolism included ALDH9A1， ASL， ASS1， PCYOX1L，， RPS28， UBE2D2， UBXN1， B3GNT1， GCNT1， and PPP1R3C， manifested as decreased amino acid metabolism that may affect the biologic processes such as autonomic nerve， urea cycle， etc.， reduced protein synthesis， increased ubiquitination of fault fold proteins， and decreased post translated modification of glycosylation and dephosphorylation. Genes related to carbohydrate metabolism included PPP1R3C， B3GNT1， and GCNT1， manifested as decreased glucogen and glycan syntheses. Genes related to nucleic acid metabolism included RMI1， SMARCD3， and PARP1， manifested as degraded DNA duplication and transcription， and increased DNA damage repair. Conclusions The metabolisms of the lipids， protein， carbohydrate， and nucleic acid in chronic superficial gastritis patients of SS obviously decreased， manifested mainly as down regulated enzyme gene expression. We inferred that these might be one of the vital pathogenesis mechanisms for nutrition dysmetabolism of SS.

  本文關(guān)鍵詞：慢性淺表性胃炎脾虛證患者與健康人物質(zhì)能量代謝基因差異表達(dá)研究，由筆耕文化傳播整理發(fā)布。