Research progress on induced autophagy for the treatment of oral cancer / 口腔疾病防治

@#Oral cancer has a high degree of malignancy, easily recurs, readily metastasizes and poor progonsis. Autophagy is a catabolic process induced in cells under stressful conditions. In recent years, studies have found that the activation of autophagy in epithelial cells can inhibit carcinogenesis and activate pathways such as mTOR and MAPK to activate autophagy in oral cancer cells and inhibit their survival. Inducing autophagy can degrade eukaryotic initiation factor 4E protein and inhibit oral cancer metastasis. Inducing autophagy in oral cancer cells can inhibit their proliferation and promote their apoptosis. Adding autophagy inducers to the treatment can help improve its efficacy and patient survival compared with chemoradiotherapy alone. In addition, the induction of autophagy in oral cancer cells can improve the body's immune function and enhance the efficacy of oral cancer immunotherapy. This article summarizes the relationship between autophagy and oral cancer and the role of induced autophagy in the treatment of oral cancer with the combined application of chemoradiotherapy and immunotherapy. The goal is to provide new ideas for inducing autophagy during the treatment of oral cancer, improving the therapeutic effect of oral cancer and the survival rate of patients. At present, the mechanism of action of induced autophagy in the treatment of oral cancer is not clear. Future research should study its mechanism of action, improve its therapeutic effect on oral cancer and develop autophagy inducers to accurately regulate and induce autophagy during the treatment of oral cancer.

Propofol exerts anti-inflammatory effects in rats with lipopolysaccharide-induced acute lung injury by inhibition of CD14 and TLR4 expression

We investigated the effect of propofol (Prop) administration (10 mg kg-1 h-1, intravenously) on lipopolysaccharide (LPS)-induced acute lung injury and its effect on cluster of differentiation (CD) 14 and Toll-like receptor (TLR) 4 expression in lung tissue of anesthetized, ventilated rats. Twenty-four male Wistar rats were randomly divided into three groups of 8 rats each: control, LPS, and LPS+Prop. Lung injury was assayed via blood gas analysis and lung histology, and tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) levels were determined in bronchoalveolar lavage fluid using ELISA. Real-time polymerase chain reaction was used to detect CD14 and TLR4 mRNA levels, and CD14 and TLR4 protein expression was determined by Western blot. The pathological scores were 1.2 ± 0.9, 3.3 ± 1.1, and 1.9 ± 1.0 for the control, LPS, and LPS+Prop groups, respectively, with statistically significant differences between control and LPS groups (P < 0.05) and between LPS and LPS+Prop groups (P < 0.05). The administration of LPS resulted in a significant increase in TNF-α and IL-1β levels, 7- and 3.5-fold, respectively (P < 0.05), while treatment with propofol partially blunted the secretion of both cytokines (P < 0.05). CD14 and TLR4 mRNA levels were increased in the LPS group (1.48 ± 0.05 and 1.26 ± 0.03, respectively) compared to the control group (1.00 ± 0.20 and 1.00 ± 0.02, respectively; P < 0.05), while propofol treatment blunted this effect (1.16 ± 0.05 and 1.12 ± 0.05, respectively; P < 0.05). Both CD14 and TLR4 protein levels were elevated in the LPS group compared to the control group (P < 0.05), while propofol treatment partially decreased the expression of CD14 and TLR4 protein versus LPS alone (P < 0.05). Our study indicates that propofol prevents lung injury, most likely by inhibition of CD14 and TLR4 expression.