Objective To study on the effects and mechanisms of ganoderma lucidum polysaccharides(GLP)on enteritis induced by enterotoxigenic Escherichia coli(ETEC)in mice.Methods Twenty-four 6-to 8-weeks-old male SPF Kunming mice were selected.A mouse enteritis model was induced by intraperitoneal injection of ETEC bacterial suspension.Mice were divided into normal group,ETEC infection group,ETEC infection+high-dose GLP group,and ETEC infection+ow-dose GLP group using a random number table method,six mice in each group.Pathological changes in mice small intestine tissue were observed through HE staining.The expression of C-reactive protein(CRP),tumor necrosis factor-(TNF)-α,and interleukin(IL)-6 proteins in mice small intestine tissues were detected by Western blot method,and expression levels of Toll-like receptor 4(TLR4),nuclear factor-KB(NF-κB)p65,and myeloid differentiation factor 88(MyD88)mRNA in mice small intestine tissues were detected by RT-qPCR technique to explore the regulatory effect of GLP on ETEC-induced mice intestinal inflammation through TLR4/NF-κB signaling pathway.Results Compared with control group,mice infected with ETEC showed lethargy,reduced appetite,damaged intestinal villi,significant inflammatory infiltration in tissues,and an increasing trend in disease activity index(DAI)scores(P＜0.05).The relative expression levels of TLR4,NF-κB p65,and MyD88 mRNA,as well as protein expression levels of CRP,TNF-α,and IL-6 in small intestine tissues of mice,were significantly increased(P＜0.01).Compared with ETEC-infected group,mice in different dosage groups showed improvements in mental status and appetite.The relative expression levels of TLR4,NF-κB p65,and MyD88 mRNA in small intestine tissues of mice were significantly decreased in all dosage groups(P＜0.01).In ETEC infection+high-dose group,protein expression levels of CRP,TNF-α,and IL-6 in small intestine tissues of mice were significantly decreased(P＜0.01),while the decrease in ETEC infection+low-dose group was not significant(P＞0.05).Compared with ETEC infection+low-dose group,ETEC infection+high-dose group showed significant decreases in relative expression levels of TLR4 and MyD88 mRNA,as well as in protein expression level of IL-6 in small intestine tissues of mice(P＜0.01 or P＜0.05).Conclusion GLP can effectively relieve intestinal inflammation induced by ETEC,and may exert its anti-inflammatory effect through regulating TLR4/NF-κB signaling pathway,which may be proportional to its concentration.

Objective To study on the effects and mechanisms of ganoderma lucidum polysaccharides(GLP)on enteritis induced by enterotoxigenic Escherichia coli(ETEC)in mice.Methods Twenty-four 6-to 8-weeks-old male SPF Kunming mice were selected.A mouse enteritis model was induced by intraperitoneal injection of ETEC bacterial suspension.Mice were divided into normal group,ETEC infection group,ETEC infection+high-dose GLP group,and ETEC infection+ow-dose GLP group using a random number table method,six mice in each group.Pathological changes in mice small intestine tissue were observed through HE staining.The expression of C-reactive protein(CRP),tumor necrosis factor-(TNF)-α,and interleukin(IL)-6 proteins in mice small intestine tissues were detected by Western blot method,and expression levels of Toll-like receptor 4(TLR4),nuclear factor-KB(NF-κB)p65,and myeloid differentiation factor 88(MyD88)mRNA in mice small intestine tissues were detected by RT-qPCR technique to explore the regulatory effect of GLP on ETEC-induced mice intestinal inflammation through TLR4/NF-κB signaling pathway.Results Compared with control group,mice infected with ETEC showed lethargy,reduced appetite,damaged intestinal villi,significant inflammatory infiltration in tissues,and an increasing trend in disease activity index(DAI)scores(P＜0.05).The relative expression levels of TLR4,NF-κB p65,and MyD88 mRNA,as well as protein expression levels of CRP,TNF-α,and IL-6 in small intestine tissues of mice,were significantly increased(P＜0.01).Compared with ETEC-infected group,mice in different dosage groups showed improvements in mental status and appetite.The relative expression levels of TLR4,NF-κB p65,and MyD88 mRNA in small intestine tissues of mice were significantly decreased in all dosage groups(P＜0.01).In ETEC infection+high-dose group,protein expression levels of CRP,TNF-α,and IL-6 in small intestine tissues of mice were significantly decreased(P＜0.01),while the decrease in ETEC infection+low-dose group was not significant(P＞0.05).Compared with ETEC infection+low-dose group,ETEC infection+high-dose group showed significant decreases in relative expression levels of TLR4 and MyD88 mRNA,as well as in protein expression level of IL-6 in small intestine tissues of mice(P＜0.01 or P＜0.05).Conclusion GLP can effectively relieve intestinal inflammation induced by ETEC,and may exert its anti-inflammatory effect through regulating TLR4/NF-κB signaling pathway,which may be proportional to its concentration.

Objective:To explore the influencing factors of psychological distress in breast cancer patients undergoing radiotherapy.Methods:A total of 177 breast cancer patients who were treated in Linyi Cancer Hospital from July 2017 to August 2020 were selected by the convenient sampling method. According to Distress Management (DM) Scale score, they were divided into no psychological distress group ( n=92) and psychological distress group ( n=85) . Binomial logistic regression analysis was used to explore the influencing factors of psychological distress in breast cancer patients. Results:The results of binomial logistic regression analysis showed that age, education level, monthly family income, payment method of medical expenses, complications and social support were the influencing factors of psychological distress ( P<0.05) . Conclusions:Breast cancer patients undergoing radiotherapy may experience psychological distress due to the influence of social support, age, monthly income, educational level and complications. Carrying out risk-based cancer care plans for these factors can improve psychological state and reduce psychological distress of patients.