KGF对电离辐射后十二指肠中CTGFBcl-2基因表达的影响

The influence of KGF on CTGF and Bcl-2 gene in duodenal tissue induced by radiation

  • 摘要:
    目的 观察角质细胞生长因子(KGF)对电离辐射后十二指肠结缔组织生长因子(CTGF)、凋亡相关基因Bcl-2表达的影响,初步探讨KGF在肠道损伤中的分子机制。
    方法 将昆明小鼠按随机数表法分为对照组、照射组、治疗组,每组10只。对照组不给予照射,照射组与治疗组给予剂量率为0.678 Gy/min、吸收剂量8 Gy的腹腔γ射线照射;治疗组在照射前2 d及照射后3 d均腹腔注射KGF,给药量为6 mg/kg。照射后第15天处死小鼠,取十二指肠组织做病理切片并观察病理表现;采用荧光定量PCR方法检测十二指肠组织中KGFCTGFBcl-2基因的表达水平。计量资料以x±s表示;两组间差异采用独立样本t检验,P < 0.05表示差异有统计学意义。
    结果 对照组十二指肠肠绒毛、隐窝结构完整,排列整齐;照射组十二指肠出现绒毛萎缩、变短或脱落,部分腺窝和绒毛处可见少量凋亡细胞;治疗组肠绒毛组织结构完整,腺窝可见少量凋亡细胞。照射组十二指肠组织中KGFCTGFBcl-2基因表达量上调,与对照组相比差异具有统计学意义(t=-125.55、-6.55、-6.69,均P < 0.05)。与照射组相比,治疗组CTGF基因表达量显著下调、Bcl-2基因表达量显著上调,差异均有统计学意义(t=4.89,-20.96,均P < 0.05)。
    结论 KGF可能通过下调CTGF基因修复电离辐射造成的损伤,并且可能通过调节Bcl-2凋亡相关基因的表达水平来降低细胞凋亡。

     

    Abstract:
    Objective To observe the effects of keratinocyte growth factor(KGF) on connective tissue growth factor(CTGF) and B-cell lymphoma 2(Bcl-2) gene expressions in radiation-induced duodenal tissue, and to investigate the molecular mechanism of KGF in radiation-induced intestinal injuries.
    Methods Using the stochastic indicator method, Kunming mice were randomly divided into control, radiation, and treatment groups, each with 10 mice. The control group did not undergo the radiation process. The radiation group and treatment group underwent abdominal cavity irradiation with a dose rate of 0.678 Gy/min and an absorbed dose of 8 Gy with γ-ray. For 2 d before and 3 d after irradiation, KGF with a dose of 6 mg/kg was administered via intraperitoneal injection to the KGF treatment group. All mice were executed 15 d after irradiation, after which the duodenal tissue pathological slices were captured. Quantitative polymerase chain reaction was used to detect the KGF, CTGF, and Bcl-2 gene relative expressions in duodenal tissue. The measurement data were x±s. The two groups were compared using independent samples t-test, and P < 0.05 indicated that the difference was statistically significant.
    Results For the control group, the duodenum intestinal villus and crypt structure were complete. For the radiation group, villi atrophy was shorter or fell off, and parts of the crypt and villi were observed in few apoptotic cells. For the treatment group, the organizational structure was complete, and a small amount of crypt can be seen in apoptotic cells. Compared with the control group, KGF, CTGF, and Bcl-2 gene expressions significantly increased after irradiation(t=-125.55, -6.55, -6.69, all P < 0.05). Compared with the radiation group, the gene expression of CTGF was significantly down-regulated(t=4.89, P < 0.05), and that of Bcl-2 was significantly up-regulated in the treatment group(t=-20.96, P < 0.05).
    Conclusions The model of acute radioactive duodenitis was successfully established. KGF repair damage was caused by ionizing radiation through down-regulating CTGF gene, and reduce apoptosis was caused by the regulation of the expression levels of the apoptosis-related Bcl-2 gene.

     

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