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目的探讨苯肾上腺素预处理对放射损伤早期大鼠颌下腺RT1-A表达的影响。方法取Wistar大鼠27只,随机分为空白对照组、单纯照射组及苯肾上腺素预处理组。预处理组大鼠于照射前半小时腹腔注射苯肾上腺素5mg/kg。应用直线加速器给予大鼠颌下腺区域20Gy X射线照射。照射后7天取大鼠颌下腺组织,应用免疫组织化学法检测各组大鼠颌下腺RT1-A(小鼠抗人HLAⅠ单克隆抗体,抗体浓度为1:200)的定位与表达;应用半定量逆转录聚合酶链法(reverse transcription-polymerase chain reaction,RT-PCR)检测各组大鼠颌下腺RT1-A mRNA的表达。结果免疫组织化学结果显示:在空白对照组RT1-A主要表达于腺泡细胞及导管细胞的胞浆和胞膜;单纯照射组RT1-A在腺泡细胞胞膜和细胞间质的表达增加;而苯肾上腺素预处理组RT1-A在腺泡细胞胞膜及间质的表达较单纯照射组明显减少。RT-PCR结果显示:单纯照射组RT1-A mRNA的表达较空白对照组增加了40.14%(P<0.05),苯肾上腺素预处理组RT1-A mRNA的表达较单纯照射组下降了45.02%(P<0.05)。结论放射线照射损伤早期可使大鼠颌下腺RT1-A的表达增加,苯肾上腺素能够下调放射损伤后RT1-A的表达,提示a1-肾上腺素受体活化参与了颌下腺放射损伤后免疫调节,为探寻防治颌下腺放射损伤的方法提供了新策略。
Objective To investigate the effect of phenylephrine preconditioning on the expression of RT1-A in the submandibular gland of rats during early radiation injury. Methods Twenty-seven Wistar rats were randomly divided into blank control group, simple irradiation group and phenylephrine pretreatment group. Pretreatment group rats were injected intraperitoneally with phenylephrine 5 mg / kg half an hour before irradiation. A linear accelerator was used to irradiate 20 Gy of rat submandibular gland. The submandibular gland tissues of rats were taken 7 days after the irradiation. Immunohistochemistry was used to detect the localization and expression of the submandibular gland RT1-A (mouse anti-human HLA-I monoclonal antibody with antibody concentration of 1: 200) in each group. Reverse transcription-polymerase chain reaction (RT-PCR) was used to detect the expression of RT1-A mRNA in the submandibular gland of rats in each group. Results The results of immunohistochemistry showed that RT1-A was mainly expressed in the cytoplasm and membrane of acinar cells and ductal cells in the blank control group. The expression of RT1-A in the membrane and interstitial of acinar cells increased in the group of irradiation alone. The phenylephrine pretreatment group RT1-A in the acinar cell membrane and interstitial expression was significantly reduced compared with the irradiation group. The results of RT-PCR showed that the expression of RT1-A mRNA was increased by 40.14% (P <0.05) compared with the blank control group, while the expression of RT1-A mRNA in the pretreated group decreased by 45.02% P <0.05). CONCLUSIONS: The expression of RT1-A in rat submandibular gland may be increased during early radiation exposure. Phenylephrine may down-regulate the expression of RT1-A after radiation injury, suggesting that a1-adrenergic receptor activation is involved in immune regulation after radiation injury in the submandibular gland. Prevention of submandibular radiation damage methods provide a new strategy.