OBJECTIVES: To investigate the effect of Scleromitrion diffusum on gastric mucosal epithelial-mesenchymal transition (EMT) in rats with gastric precancerous lesion. METHODS: Fifty SD rats were randomly divided into blank control group (n=11), model control group (n=13), Scleromitrion diffusum (SD) group (n=13) and vitase group (n=13). Gastric precancerous lesion animal model was prepared by 1-methyl-3-nitro-1-nitrosoguanidine complex polyfactor method, and the drugs were administrated by gavage once a day for 6 weeks. The pathological changes of gastric mucosa were observed with hematoxylin and eosin staining, the expression of EMT marker proteins were detected with immunohistochemical staining and Western blotting. RESULTS: Compared with the model control group, the gastric mucosal injury was significantly attenuated in the Scleromitrion diffusum group, the mucosal tissue structure gradually recovered, the saccular expansion area was reduced, and the inflammatory infiltration was ameliorated. The expression of epithelial cadherin was higher, and the expression of neural cadherin and vimentin in the Scleromitrion diffusum group were lower than those of model control group (all P<0.05). CONCLUSIONS Scleromitrion diffusum can ameliorate gastric mucosal injury in rats with gastric precancerous lesion by reversing the EMT.
Animals ; Rats ; Rats, Sprague-Dawley ; Epithelial-Mesenchymal Transition/drug effects* ; Precancerous Conditions/metabolism* ; Gastric Mucosa/metabolism* ; Stomach Neoplasms/drug therapy* ; Male ; Cadherins/metabolism*

[This corrects the article DOI: 10.1016/j.apsb.2022.05.019.].

Objective To explore the functions of β-glucan-induced extracellular vesicles(EVs)released from J774A.1 cells.Methods EVs were extracted from the culture supernatant of J774A.1 cells,which were cultured with or without β-glucan,using differential centrifugation.The phenotype of extracellular vesicles was identified by transmission electron microscopy(TEM),nano-particle tracking analysis(NTA)and Western blotting(WB).The peritoneal macrophages(PMs)were harvested from C57BL/6J mice,and incubated with the control EVs(C-EVs)and theβ-glucan-induced EVs(G-EVs).Total RNA was extracted from the PMs and reversely transcribed to cDNA.The expression levels of the macrophage polarization-related genes were detected through real-time fluorescence quantitative PCR(qRT-PCR).Meanwhile,the culture supernatant of the PMs was collected and assayed by enzyme-linked immunosorbent assay(ELISA)to detect the expression levels of proinflammatory cytokines tumor necrosis factor-α(TNF-α)and interleukin-6(IL-6).Results EVs of the control(C-EVs)and those from the β-glucan-induced(G-EVs)were isolated from J774A.1 cell culture medium.The results of TEM analysis showed that EVs had a membrane wrapped structure and the particle diameters ranged from 100 to 1000 nm.The NTA results showed that the average particle sizes were 162.4 and 175.6 nm respectively.The results of WB assay showed the expressions of characterized marker molecules such as CD81,CD9,CD63 and TSG101 were detected.qRT-PCR results showed that the expression levels of M1 polarization related genes such as Tnfa and inos were significantly increased in PM cells of the C-EVs treatment group,but those in the G-EVs treatment group were significantly lower than in the C-EVs treatment group.Meanwhile,the expression levels of M2 polarization indicators Cd206 and Arg-1 in the C-EVs treatment group were significantly decreased,while those in the G-EVs treatment group were significantly higher than those in C-EVs treatment group.Accordingly,the results of ELISA showed that the expression levels of TNF-α and IL-6 in the conditioned medium of the C-EVs treatment group were significantly increased,while those in the G-EVs treatment group were significantly lower than in the C-EVs treatment group.Conclusion Compared with the natural EVs from J774A.1 cells,the ability of β-glucan-induced EVs to drive M1 polarization of macrophages isdramatically compromised,with much fewer proinflammatory cytokines released,suggesting that β-glucan might contribute to immune regulation through EVs.

The immune system is the defender of human health,whose dysregulation is the source of various diseases.Re-duced immune defense and immune surveillance capabilities lead to difficulties in removing pathogens and malignant cells,thus increasing morbidity and mortality risk.Stress is a major factor in the decline of the immune system.In past studies,it has been demon-strated both in animal and humans that stress increases the levels of neuroendocrine hormones in the body,particularly glucocorticoids and catecholamines.Through the action of these stress hormones,stress has a number of detrimental effects on immune function,and this review combs through the progress of research on the regulation of immune cells by glucocorticoids.

Objective To study the application effect of quality control circle(QCC)in reducing the dissatisfaction rate of physical examination clients in health management center.Methods To establish QCC,selected the health check-up popula-tion in our hospital in September-2019 and March-2020,through the questionnaire investigation and analysis,compare the dis-satisfaction of the clients before and after the quality control circle.Results After carrying out QCC activities,the dissatisfaction of physical examination clients was significantly lower than that before QCC,and the difference was statistically significant(P＜0.05).Conclusion The activities of QCC in the health management center can effectively improve the quality of the physical examination work and reduce the dissatisfaction of the customers in the physical examination.It is of great significance to the health management.

Objective To evaluate the therapeutic effect of Huangqin Decoction(HQD)on ulcerative colitis(UC)in mice and explore its mechanism.Methods Male Balb/c mice were randomly divided into normal control group,model group,mesalazine group(5-ASA,200 mg/kg),and low-,medium-and high-dose HQD groups(2.275,4.55 and 9.1 g/kg,respectively).With the exception of those in the normal control group,all the mice were exposed to 3%DSS solution in drinking water for 7 days to establish UC models.After treatment with the indicated drugs,the mice were assessed for colon injury and apoptosis using HE,AB-PAS and TUNEL staining,and the expression levels of inflammatory factors were detected with ELISA.Western blotting,immunohistochemistry and qRT-PCR were used to detect the changes in protein expressions associated with the intestinal chemical barrier,mechanical barrier and endoplasmic reticulum stress(ERS).Results HQD treatment significantly reduced DAI score and macro score of UC mice,decreased colonic epithelial cell apoptosis,lowered expressions of IL-6,TNF-α,IL-1β and IL-8,and enhanced the expressions of MUC2 and TFF3.HQD treatment also upregulated the protein expressions of claudin-1,occludin and E-cadherin,reduced the expressions of GRP78,CHOP,caspase-12 and caspase-3,decreased the phosphorylation levels of PERK,eIF2α and IRE1α,and increased the Bcl-2/Bax ratio in the colon tissues of UC mice.Conclusion HQD inhibits colonic epithelial cell apoptosis and improves intestinal barrier function in UC mice possibly by reducing ERS mediated by the PERK and IRE1α signaling pathways.

Objective To evaluate the therapeutic effect of Huangqin Decoction(HQD)on ulcerative colitis(UC)in mice and explore its mechanism.Methods Male Balb/c mice were randomly divided into normal control group,model group,mesalazine group(5-ASA,200 mg/kg),and low-,medium-and high-dose HQD groups(2.275,4.55 and 9.1 g/kg,respectively).With the exception of those in the normal control group,all the mice were exposed to 3%DSS solution in drinking water for 7 days to establish UC models.After treatment with the indicated drugs,the mice were assessed for colon injury and apoptosis using HE,AB-PAS and TUNEL staining,and the expression levels of inflammatory factors were detected with ELISA.Western blotting,immunohistochemistry and qRT-PCR were used to detect the changes in protein expressions associated with the intestinal chemical barrier,mechanical barrier and endoplasmic reticulum stress(ERS).Results HQD treatment significantly reduced DAI score and macro score of UC mice,decreased colonic epithelial cell apoptosis,lowered expressions of IL-6,TNF-α,IL-1β and IL-8,and enhanced the expressions of MUC2 and TFF3.HQD treatment also upregulated the protein expressions of claudin-1,occludin and E-cadherin,reduced the expressions of GRP78,CHOP,caspase-12 and caspase-3,decreased the phosphorylation levels of PERK,eIF2α and IRE1α,and increased the Bcl-2/Bax ratio in the colon tissues of UC mice.Conclusion HQD inhibits colonic epithelial cell apoptosis and improves intestinal barrier function in UC mice possibly by reducing ERS mediated by the PERK and IRE1α signaling pathways.

This study was designed to investigate the role of ring finger protein 20(RNF20)in host innate immunity against RNA viruses.Dual luciferase reporter assay was employed to examine the effects of RNF20 overexpression on Sendai virus(SeV)infection-induced activation of interferon a4(Ifna4)gene promoter in 293T human embryonic kidney epithelial cells.Rnf20 myeloid conditional knockout mouse model was constructed(Rnf2OF/F;Lyz2-Cre),and the frequency of myeloid subsets in the bone marrow,spleen,blood of Rnf20F/F;Lyz2-Cre mice and littermate Rnf20F/F mice were detected by flow cytometry.After bone marrow-derived macrophages(BMDMs)were cultured and subjected to the infection of SeV and vesicular stomatitis virus(VSV),Western blot was used to detect the phosphorylation of transcription factor interferon regulatory factor 3(IRF3)and nuclear factor-κB(NF-κB).ELISA was used to detect the production of IFN-β,TNF-α and IL-6,and Bulk RNA-sequencing was employed to explore transcriptional changes.Furthermore,M1 and M2 macrophage polarization was induced by LPS and IL-4,respectively,to confirm the changes revealed by transcriptome analysis.Data showed that RNF20 overexpression showed no significant effect on SeV infection-induced activation of Ifna4 gene promoter in 293T cells.There is almost no difference in the development of myeloid subsets between Rnf20F/F;Lyz2-Cre and Rnf2OF/F mice.After RNA viral infection of BMDMs from Rnf20F/F;Lyz2-Creand Rnf201 mice,the phosphorylation of IRF3 and NF-κB p65 and the expression of IFN-[3,TNF-α and IL-6 were comparable between the two groups,while the expression levels of several genes related to macrophage polarization were significantly different.The loss of RNF20 showed the tendency of hindering M1 macrophage polarization while promoting M2 macrophage polarization.In conclusion,RNF20 does not affect RNA viral infection-induced activation of IRF3 or NF-κB pathways,but it might get involved in the resolution of inflammation afterwards.

Lysinuric protein intolerance (LPI) is a rare autosomal recessive disorder involving digestive, renal, respiratory, and nervous systems caused by SLC7A7 gene mutation.It was first reported in Finland and now has been found worldwide.A total of 8 cases have been reported in China.The abnormal function of the y + amino acid transporter caused by SLC7A7 gene mutation can explain some clinical features, but the pathophysiological mechanism underlying the associated lung, kidney and blood system disorders is not clear.The varying clinical manifestations of LPI often lead to misdiagnosis or delayed diagnosis.This article reviews the pathogenesis, clinical characteristics, diagnosis and treatment of LPI, to enhance clinicians′ understanding of this disease.

Obiective:To compare characteristics of alveolar macrophages(AMs)or AM-like cells in vitro cultured from different progenitors in mice of different ages in presence of GM-CSF,TGF-β and PPAR-γ agonist rosiglitazone(in brief,GTR),according to a previously reported optimized culture procedure.Methods:After bronchoalveolar lavage fluid(BALF)and bone marrow were isolated from mice of different ages and fetal livers were isolated from embryonic-day-15～17 mice,mononuclear cells were seeded into 12-well plates and cultured in presence of GTR.Generated cells were subjected to flow cytometry analysis to analyze expressions of AM markers F4/80,CD11b,CD170 and CD11c.Results:After culture,almost all BALF-derived cells were round-shaped under light microscope,about half bone marrow-derived cells appeared round-shaped,and about 85% fetal liver-derived cells showed round-shaped morphology.Frequency of BALF-AMs from 4-week-old mice was nearly 90%.Frequency and number of BALF-AMs increased with age of mice.Number of BALF-AMs from 12-week-old mice was nearly 1×106.Frequency of bone marrow-derived AM-like cells from 4-week-old mice was lower than 20% and increased to about 40%～45% for 8-week-old and 12-week-old mice.Number of bone marrow-derived AM-like cells increased with age of mice,and about 0.8×106 cells/well bone marrow-derived AM-like cells were produced from 12-week-old mice.Frequency of fetal liver-derived AM-like cells was around 84% and their number could reach 4×106 cells/well.Conclusion:Purity and number of AMs or AM-like cells in vitro cultured from different progenitors in mice of different ages vary dramatically.Detailed condition should be chosen according to specific study requirements.