目的 觀察鼻咽清毒顆粒(BQG)對放療引起大鼠口腔黏膜損傷的保護作用,并探討其可能的作用機制。方法 采用FAT細胞皮下注射法,建立F344大鼠種植瘤模型。F344大鼠分為對照組、對照放射組、模型組、BQG低、中、高劑量(1、2、4 g·kg^-1)組。除對照組外,各組動物進行X線照射,放射劑量為10 Gy·d^-1,連續(xù)5 d。BQG 3個劑量組于第1天造模后進行藥物干預(yù),每天ig給藥1次,連續(xù)28 d;其余3組給予等體積的蒸餾水。每日對各組大鼠進行一般觀察,定期進行稱重。末次給藥后24 h處死大鼠,采集各組大鼠口腔黏膜及血漿,酶聯(lián)免疫吸附實驗(ELISA)檢測大鼠血漿中白細胞介素-6(IL-6)、白細胞介素-1β(IL-1β)、腫瘤壞死因α(TNF-α)水平;Western blotting檢測口腔黏膜NF-κB p65、p-P65、MAPK、ERK、p-ERK等蛋白表達情況,并對其進行組織病理學(xué)檢查。結(jié)果 BQG低、中、高劑量組均能提高大鼠體質(zhì)量增長率;BQG各給藥組能顯著降低口輕黏膜組織中IL-6、IL-1β、TNF-α水平(P<0.05、0.01);與模型組比較,BQG各給藥組MAPK蛋白表達顯著降低,p-p65/p65,p-ERK/ERK比值顯著降低(P<0.05、0.01)。結(jié)論 BQG對放射性口腔黏膜炎具有修復(fù)作用,其可能通過調(diào)控NF-κB/MAPK/ERK信號通路,降低口腔黏膜炎癥因子水平相關(guān)。

Objective To observe the protective effect of Biyan Qingdu Granules (BQG) on radiotherapy-induced oral mucosal injury in rats and to explore its possible mechanism of action. Methods An F344 rat implantation tumor model was established by subcutaneous injection of FAT cells. F344 rats were divided into the control group, control radiation group, model group, and BQG low, medium, and high dose (1, 2, and 4 g·kg^-1) groups. Except for the control group, the animals in each group were subjected to Xray irradiation at a radiation dose of 10 Gy·d^-1 for five consecutive days. Three dose groups of BQG were subjected to pharmacological intervention after the first day of modeling, and the drug was administered by gavage once a day for 28 consecutive days. The remaining three groups were given equal volumes of distilled water. The rats in each group were subjected to general observation daily and weighed periodically. The rats were executed 24 h after the last administration. The oral mucosa and plasma of rats in each group were collected. The enzyme-linked immunosorbent assay (ELISA) detected interleukin-6 (IL-6), interleukin 1β (IL-1β), and tumor necrosis factor α (TNF-α) in the plasma of rats. Western blotting detected the oral mucosa NF-κB p65, p-P65, MAPK, ERK, p-ERK, and other protein expression, and histopathological examination. Results The low, medium, and high dose groups of BQG could increase the body weight growth rate of rats; The administration groups of BQG could significantly reduce the levels of IL-6, IL-1β, and TNF-α in the tissues of the oral light mucous membranes (P < 0.05, 0.01, respectively). Compared with the model group, the administration groups of BQG could significantly reduce the protein expression of MAPK, and the ratios of p-p65/p65, p-ERK/ERK ratio were significantly reduced (P < 0.05, 0.01). Conclusion BQG have a therapeutic effect on radioactive oral mucositi, which may be related to reducing the level of oral mucosal inflammatory factors by regulating the NF-κB/MAPK/ERK signaling pathway.

R285.5

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