Objective To analyze the effects of target volume optimization on oral mucosal reaction and salivary gland function in oropharyngeal cancer patients receiving intensity-modulated radiotherapy(IMRT).Methods A total of 120 patients with oropharyngeal cancer admitted to Affiliated Hospital of Jiangsu University from April 2020 to August 2022 were selected and randomly grouped into control group(n=60,conventional IMRT)and treatment group(n=60,cervical region Ⅱ and the oral target region were optimized during IMRT).The therapeutic efficacy,parotid gland dose,incidence of acute oral mucosal reaction,dry mouth and oral pain at 3 months after IMRT were compared between two groups.The resting-state apparent diffusion coefficient(ADC)values of parotid and submandibular glands at different time points(before radiotherapy,the 4th week of radiotherapy,the end of radiotherapy and 3 months after radiotherapy)were recorded.Results The difference in the objective reaction rate between two groups was trivial[80.00％(48/60)vs 75.00％(45/60),P>0.05].The mean dose(Dmean)and V34 of the unaffected parotid gland and the Dmean and V30 of the oral cavity in treatment group were lower than those in control group(P<0.05).The incidences of acute oral mucosal reaction,dry mouth and oral pain at 3 months after radiotherapy in treatment group were 41.67％,50.00％,and 58.33％,lower than those in control group(75.00％,78.33％,and 85.00％)(P<0.05).The resting-state ADC values of parotid and submandibular glands at the 4th week of radiotherapy,the end of radiotherapy,and 3 months after radiotherapy in both two groups were higher than those before radiotherapy(P<0.05).At the 4th week of radiotherapy,the end of radiotherapy,and 3 months after radiotherapy,the resting-state ADC values of parotid and submandibular glands in treatment group were lower than those in control group(P<0.05).Conclusion Optimizing target volume during oropharyngeal IMRT can effectively prevent the occurrence of radiation-induced mucositis,alleviate oral mucosal reaction,oral pain and dry mouth,reduce parotid gland dose,and diminish the effects of IMRT on salivary gland function in patients.

【Objective】 To investigate the cell death-inducing effect of methyl rosmarinate (MR) on human hepatoma Hep-3B and SK-Hep1 cells and their potential mechanisms. 【Methods】 The effects of MR on the viability of Hep-3B, SK-Hep1 and MIHA cells were determined by cell counting kit-8 (CCK-8) assay. The morphological changes of three kinds of cells treated with different concentrations of MR were observed by optical microscopy. EdU assay and flow cytometry were used to detect the proliferation and apoptosis of Hep-3B and SK-Hep1 cells. Transwell assay was used to study the effects of MR on the migration and invasion of Hep-3B and SK-Hep1 cells. Western blotting was used to evaluate the protein expression levels of apoptosis, EMT and Akt/mTOR signaling pathways. 【Results】 After treated with different concentrations of MR (0~200 μmol/L) for 48 h, Hep-3B and SK-Hep1 cells activities were significantly decreased in a concentration-dependent manner (P<0.01), while there was no significant effect on MIHA cell activity (P>0.05), and the IC50 of Hep-3B and SK-Hep1 cells were 102.5 and 99.3 μmol/L, respectively. MR treatment (0-150 μmol/L) significantly inhibited the proliferation of Hep-3B and SK-Hep1 cells (P<0.05), while cell detachment and shrinkage were observed by optical microscopy on the Hep-3B and SK-Hep1 cells, while the morphology of MIHA cells was not changed. Compared with the control group, MR (100, 150 μmol/L) induced apoptosis in Hep-3B and SK-Hep1 cells, the expression levels of the pro-apoptotic proteins Bax and cleaved PARP were significantly increased (P<0.05), while the expression level of the anti-apoptotic protein Bcl-2 was significantly decreased (P<0.05). MR (100, 150 μmol/L) also inhibited the migration and invasion of HCC cells, significantly increased the expression of E-cadherin and decreased the expression of N-cadherin and Vimentin compared with the control group (P<0.05). Finally, Western blotting results showed that the expressions of p-Akt and p-mTOR in Hep-3B and SK-Hep1 treated by MR were significantly reduced in a dose-dependent manner, suggesting that MR may play an anti-cancer role by inhibiting Akt/mTOR signaling pathway. 【Conclusion】 MR can promote apoptosis in Hep-3B and SK-Hep1 cells, which may be closely related to the inhibition of Akt/mTOR signaling pathway.