AIM:To investigate the mechanism of action of Wenweiyang decoction(WWYD)in treating func-tional dyspepsia in rats based on mast cell activation and stem cell factor(SCF)/receptor tyrosine kinase c-Kit signaling pathway.METHODS:Sixty SD rats were randomly divided into control group,model group,ranitidine hydrochloride capsule group,and low-,medium-and high-dose WWYD groups,with 10 rats in each group.The rat model of functional dyspepsia was established by tail clamping and irregular feeding compound senna method.After modeling,the rats in con-trol group and model group were given normal saline,while those in low-,medium-and high-dose(0.743 g/mL,1.485 g/mL and 2.970 g/mL)WWYD groups and ranitidine hydrochloride capsule(3 g/L)group were treated with corresponding drugs by intragastric administration.After treatment,the propulsion rate of the small intestine was measured by the carbon ink propulsion method.Rat duodenal mast cells were observed and counted by toluidine blue staining.ELISA was used for determination of mast cell tryptase(MCT)and histamine(HA)content in rat duodenum.The mRNA levels of SCF and c-Kit in duodenum were detected by RT-qPCR.Western blot and immunohistochemistry were employed to determine the ex-pression levels of SCF and c-Kit in the duodenum.RESULTS:Compared with model group,WWYD treatment signifi-cantly increased the propulsion rate of the small intestine in rats(P<0.05).ELISA results showed that WWYD reduced the number of mast cells and the content of MCT and HA in the duodenal mucosa tissue of rats(P<0.05).Western blot and immunohistochemistry results suggested that WWYD up-regulated the protein expression levels of c-Kit and SCF in the duodenal tissue of rats(P<0.05),and increased the numbers of SCF and c-Kit positive cells.RT-qPCR results indicated that WWYD up-regulated the mRNA expression of c-Kit and SCF in the duodenum of rats(P<0.05).Moreover,the small intestinal propulsion rate was negatively correlated with MCT and HA content,and positively correlated with the expres-sion of SCF and c-Kit.CONCLUSION:Wenweiyang decoction promotes rat duodenal motility,and its mechanism may be related to the inhibition of rat duodenal MCT and HA production and activation of SCF/c-Kit signaling pathway.

Objective:To understand the current situation of nurses in 52 hospitals in China on mastery of knowledge about skin injury in the elderly based on the background of mixed-mode homogenization training.Methods:Using the convenient sampling method, a total of 1 067 nurses from 52 hospitals in China were selected as the research objects in January 2021. A self-designed questionnaire on knowledge of skin injury in the elderly was used to investigate the nurses through the questionnaire star and univariate analysis was used to analyze the influencing factors. A total of 1 067 questionnaires were distributed and 1 067 valid questionnaires were recovered, and the effective recovery rate was 100%.Results:The knowledge scores of pressure injury, incontinence-associated dermatitis, skin tear and xerosis cutis among 1067 nurses were (95.66±7.37) , (95.65±9.15) , (91.37±15.45) and (87.67±15.91) , respectively. The results of univariate analysis showed that hospital grade was the influencing factor of nurses' knowledge score of pressure injury, skin tear and incontinence-associated dermatitis ( P<0.05) , educational background was the influencing factor of nurses' knowledge score of skin tear ( P<0.05) , professional title was the influencing factor of nurses' knowledge scores of pressure injury, incontinence-associated dermatitis and xerosis cutis ( P<0.05) . Conclusions:Hospitals at all levels need to strengthen the theoretical and practical knowledge training for nurses on skin xerosis and skin tear in the elderly, especially for nurses with primary titles and lower education in grassroots hospitals.

Objective:To explore the status and influencing factors of incontinence-associated dermatitis among elderly inpatients in 52 hospitals nationwide, and to analyze the nursing of elderly inpatients with incontinence, so as to provide a reference for clinical intervention.Methods:On March 31, 2021, convenience sampling was used to select 14 675 elderly inpatients from 52 hospitals across the country as the research object. The self-designed Incontinence-associated Dermatitis Questionnaire for Elderly Inpatients was used to collect general demographic data, health status, incontinence, and skin nursing. Binomial Logistic regression was used to investigate the influencing factors of incontinence-associated dermatitis in elderly inpatients.Results:Among 14 675 elderly inpatients, the prevalence rates of xerosis cutis, incontinence and incontinence-associated dermatitis were 38.78% (5 691/14 675) , 11.06% (1 623/14 675) and 1.91% (280/14 675) , respectively. The prevalence of mild, moderate and severe incontinence-associated dermatitis were 1.27% (186/14 675) , 0.55% (81/14 675) , and 0.09% (13/14 675) , respectively. Among the nursing of 1 623 elderly inpatients with incontinence, the items with low implementation rate were the use neutral lotion to clean skin (14.17%, 230/1 623) , use of skin protectant after moisturizing (17.68%, 287/1 623) , moisturizing after cleansing the skin (28.90%, 469/1 623) . The results of binomial Logistic regression analysis showed that xeroderma, fecal incontinence, urinary and fecal incontinence, ≥2 kinds of combined medication, and hospital stay >30 days were risk factors for incontinence-associated dermatitis in elderly inpatients.Conclusions:The risk factors of incontinence-associated dermatitis in elderly inpatients mainly include xerosis cutis, type of incontinence, ≥2 kinds of combined medication, and hospital stay >30 days.

Objective To study the relationship between phosphodiesterase 4D (PDE4D) gene rs966221 single nucleotide polymorphisms (SNPs) and ischemic stroke (IS) in Guangxi Zhuang population.Methods One hundred and one IS patients from Guangxi Zhuang Autonomous Region served as IS pgroup and 104 healthy subjects undergoing physical ecamination served as control group in this study.Their PDE4D gene rs966221 SNPs were detected by SNaPshot technique.The genotypes and frequencies of alleles were compared between the two groups and the relationship between PDE4D gene rs966221 SNPs and IS was analyzed.Results No significant difference was found in the GG,GA,AA genotypes and in the frequencies of G and A alleles between the two groups (0.99％ vs 3.85％,29.70％ vs 21.15％,69.31％ vs 75.00％,P＞0.05;15.84％ vs 14.42％,84.16％ vs 85.58％,P＞0.05).Univariate and multivariate logistic regression analysis showed that the PDE4D gene rs966221 SNPs were not related with the risk of IS in dominant AA vs GG+GA,recessive GG vs AA+GA and additive GG vs AA genetic models (P＞0.05).Conclusion The PDE4D gene rs966221 SNPs are not related with IS in Guangxi Zhuang population.

Chronic high-salt diet-associated renal injury is a key risk factor for the development of hypertension. However, the mechanism by which salt triggers kidney damage is poorly understood. Our study investigated how high salt (HS) intake triggers early renal injury by considering the ‘gut-kidney axis’. We fed mice 2% NaCl in drinking water continuously for 8 weeks to induce early renal injury. We found that the ‘quantitative’ and ‘qualitative’ levels of the intestinal microflora were significantly altered after chronic HS feeding, which indicated the occurrence of enteric dysbiosis. In addition, intestinal immunological gene expression was impaired in mice with HS intake. Gut permeability elevation and enteric bacterial translocation into the kidney were detected after chronic HS feeding. Gut bacteria depletion by non-absorbable antibiotic administration restored HS loading-induced gut leakiness, renal injury and systolic blood pressure elevation. The fecal microbiota from mice fed chronic HS could independently cause gut leakiness and renal injury. Our current work provides a novel insight into the mechanism of HS-induced renal injury by investigating the role of the intestine with enteric bacteria and gut permeability and clearly illustrates that chronic HS loading elicited renal injury and dysfunction that was dependent on the intestine.
Animals ; Bacteria ; Bacterial Translocation ; Blood Pressure ; Drinking Water ; Dysbiosis ; Enterobacteriaceae ; Gastrointestinal Microbiome ; Gene Expression ; Hypertension ; Intestines ; Kidney ; Mice* ; Microbiota ; Permeability ; Risk Factors

AIM:To investigate the inhibitory effect of PDE4 inhibitor rolipram on the releases of inflammatory cytokines in mouse macrophages (RAW264.7 cells) induced by myeloid-related protein 8/14 (MRP8/14), and to explore the role of nuclear factor-κB (NF-κB) in this process.METHODS:RAW264.7 cells were treated with MRP8/14.The inflammatory cytokines TNF-α and IL-6 were determined by LiquiChip and qPCR.In contrast, RAW264.7 cells were pretreated with rolipram prior to MRP8/14 exposure.After MRP8/14 challenge, the inflammatory cytokines TNF-α and IL-6 were determined by LiquiChip and qPCR.Moreover, the phosphorylation level of NF-κB P65 was determined by Western blot.The nuclear translocation of NF-κB P65 in RAW264.7 cells was detected by indirect immunofluorescence.RESULTS:The results of LiquiChip and qPCR showed that MRP8/14 enhanced the expression of TNF-α and IL-6 (P<0.01),while pretreatment with rolipram markedly down-regulated the level of inflammatory cytokines induced by MRP8/14 (P<0.05).Meanwhile, MRP8/14 significantly activated the phosphorylation of NF-κB P65, and the protein expression of p65 in the nucleus was increased,while pretreatment with rolipram suppressed the phosphorylation of NF-κB P65 induced by MRP8/14.CONCLUSION:Rolipram may significantly reduce the releases of the inflammatory cytokines induced by MRP8/14 through the NF-κB signaling.

AIM:To explore the effects of stanniocalcin 2 (STC2) on the proliferation, migration and the process of epithelial-mesenchymal transition (EMT) in human hepatocellular carcinoma HepG2 cells.METHODS:The expression levels of STC2 in the hepatocellular carcinoma cell lines and normal liver cells were assessed by Western blot.Colony formation assay was used to test the effect of STC2 on the proliferation of HepG2 cells.The effects of STC2 on the expression of proliferation-related molecules at mRNA and protein levels were determined by RT-qPCR and Western blot.The effect of STC2 on the migration ability was measured by Transwell assay.The mRNA and protein levels of vimentin and E-cadherin in STC2-overexpressing and-silencing cell lines were detected by RT-qPCR and Western blot.RESULTS:Compared with the normal liver cell line, the protein expression of STC2 was up-regulated in the hepatocellular carcinoma cell lines.The results of colony formation assay indicated that STC2 promoted the proliferation of HepG2 cells.STC2 significantly regulated the proliferation-related gene expression, such as cyclin D1.The results of Transwell assay showed that STC2 enhanced the migration ability of the HepG2 cells and influenced the EMT process.CONCLUSION:STC2 promotes the proliferation of HepG2 cells and affects the expression of proliferation-related genes.STC2 influences the process of EMT and promotes the migration of HepG2 cells.

AIM:To explore the mitochondrial pathway in the apoptosis of PC3 cells induced by PXD101 (also named as belinostat).METHODS:PC3 cells were treated with PXD101 at different doses or stimulated with PXD101 for different time.The effect of PXD101 on the viability of PC3 cells was measured by CCK-8 assay.The apoptotic rates and the mitochondrial membrane potential (MMP) were analyzed by flow cytometry.The protein levels of Bcl-2, Bax and cytochrome C (Cyt C) were determined by Western blot.The caspase-3 activity were tested by caspase-3 activity assay kit.RESULTS:The viability of the PC3 cells was inhibited by PXD101 in a dose-and time-dependent manner.Flow cytometric analysis showed that the apoptotic rates were increased in the cells treated with PXD101 (P<0.01).At the same time, PXD101 induced the decreases in MMP and Bcl-2, the release of Cyt C, and the increase in caspase-3 activity.CONCLUSION:PXD101 induces the apoptosis of human prostate cancer cell line PC3 by mitochondrial signal pathway.

AIM:To investigate the effect of growth differentiation factor 11 ( GDF11 ) on the expansion of CD8 +memory stem T cells ( Tscm) and to further improve the effect of adoptive immunotherapy.METHODS:Healthy human peripheral blood mononuclear cells ( PBMCs) were isolated by density gradient centrifugation at first.Among the i-solated PBMCs, CD8 +T cells were further purified with MACS microbeads.The CD8 +T cells were then randomly divided into experimental groups and control group.The same volume of different concentrations of GDF11 were added into the ex-perimental groups, and the same volume of PBS solution was added into the control group.Finally, the expansion of Tscm in experimental groups and control group was measured by flow cytometry at several time points.RESULTS:GDF11 sig-nificantly increased the number of Tscm in CD8 +T cells in vitro expansion and also dramatically increased the ratio of Tscm in CD8 +T cells.Furthermore, 400 μg/L GDF11 treatment for 3 weeks was the optimal condition to induce CD8 +Tscm. CONCLUSION:GDF11 effectively increases the number and ratio of Tscm in the CD8 +T cells in cell culture growth, thereby creating a new strategy to further improve the efficiency of adoptive immunotherapy.

AIM:To investigate the effects of myeloid-related protein 8/14 ( MRP8/14 ) on the survival and apoptosis of human alveolar epithelial cell line A549, and to explore the role of nuclear factor-κB (NF-κB) in this process. METHODS:A549 cells were treated with different doses of MRP8/14 or stimulated with MRP8/14 for different time.The effect of MRP8/14 on the viability of A549 cells was determined by CCK-8 assay.The apoptotic rates were tested by flow cytometry.The nuclear translocation of NF-κB p65 was detected by Western blot and indirect immunofluorescence.Be-sides, the phosphorylation level of NF-κB p65 was determined by Western blot.NF-κB-specific inhibitor Bay 11-7082 was used to further analyze the role of NF-κB in the apoptosis induced by MRP8/14.RESULTS:The viability of the A549 cells was affected by MRP8/14 in a dose-and time-dependent manner.Flow cytometric analysis showed that the apoptotic rates were increased in the cells treated with MRP8/14 (P<0.01).In A549 cells administered with MRP8/14, NF-κB p65 was significantly phosphorylated and translocated into the nuclei, suggesting the activation of NF-κB signaling pathway. However, NF-κB-specific inhibitor Bay 11-7082 significantly attenuated the cell apoptosis induced by MRP8/14 ( P <0.01).CONCLUSION:NF-κB plays an important role in regulating the apoptosis of human alveolar epithelial cells in-duced by MRP8/14.