Acta Universitatis Medicinalis Anhui

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Anhui Provincial Education Department

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Anhui Medical University

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Weng Jianping

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ISSN 1000 - 1492

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Astragalus polysaccharide regulates exosomes derived from breast cancer cells and its effects on macrophage polarization and antitumor effects

Guan Chenjuan; Xie Caixia; Zheng Xiaojiao; Bao Nana; Wang Lu; Bai Wenhui; Qiao Shu; Zhang Haonan

DOI: 专辑：医药卫生科技

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abstract:
Objective To investigate the effects and mechanisms of Astragalus Polysacharin (APS) on the proliferation and metastasis of breast cancer cells by regulating miR-107 and miR-346-mediated macrophage polarization in breast cancer-derived exosomes. Methods Forty 8-week-old female BALB/c mice were selected and breast cancer xenograft models and 4T1 transplanted tumor models were established. The mice were divided into the control group and the APS group. The APS group mice received daily intragastric administration of APS for 25 days, while the control group mice were given the same amount of normal saline. After all treatments were completed, the mice were euthanized, and tumor tissues were isolated. Western blot and flow cytometry were used to detect the expressions of proliferating cell nuclear antigen (PCNA), Ki-67, CD206, CD163, inducible nitric-oxide synthase (iNOS), and CD86. The apoptosis of single-cell suspensions in tumor tissues was analyzed. Human breast cancer cell line MDA-MB-231 was cultured and stimulated with APS, and exosomes from the cell culture medium were collected. The proliferation, migration, and invasion of cells were detected by CCK-8 assay, scratch assay, permeability chamber cell invasion assay, and qRT-PCR. Differentially expressed genes were screened by bioinformatics. ResultsBy measuring the expressions of molecules related to breast cancer cell proliferation and metastasis, it was shown that APS treatment reduced the expressions of proliferation-related proteins (PCNA and Ki-67) and metastasis-related proteins (Vimentin) in MDA-MB-231 xenograft tumor tissues; and the polarization of tumor-associated macrophages was observed. APS treatment of 4T1 transplanted tumor tissues could reduce the number of M2 macrophages and increase the number of M1 macrophages, resulting in an increase in the ratio of M1/M2 macrophages and an increase in cell apoptosis in 4T1 transplanted tumor tissues. The expressions of related proteins iNOS and CD86 increased, and CD206 and CD163 decreased. After APS treatment, the exosomes produced by MDA-MB-231 reduced the polarization of M2 macrophages and affected the expressions of miR-107 and miR-346. Conclusion APS inhibits the polarization of M2 macrophages by regulating the expression of miR-107 or miR-346 in breast cancer cell-derived exosomes, ultimately inhibiting the proliferation and metastasis of breast cancer cells.

Experimental study on the improvement of non-alcoholic fatty liver disease by regulating G0S2 and ATGL expression with polydatin

Sheng Luguang; Liu Dandan; Liu Weibin; Lei Tao; Chen Qingguang; Lu Hao; Xu Bilin

DOI: 专辑：医药卫生科技

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abstract:
Objective To investigate the effects of polydatin on a high-fat diet-induced non-alcoholic fatty liver disease (NAFLD) mouse model and hepatoma G2 (HepG2) cell model, and to reveal its potential molecular mechanisms. MethodsThirty 6-week-old male SPF C57BL/6J mice were randomly divided into a normal diet group and a high-fat diet group. After the NAFLD mouse model was established in the high-fat diet group, they were further divided into a model group and a polydatin treatment group. The polydatin treatment group was administered polydatin by gavage at a dose of 250 mg/(kg·d) for 10 weeks, during which body weight was monitored and oral glucose and insulin tolerance tests were performed. At the end of the experiment, a series of tests to evaluate the effects of polydatin on mouse liver weight, blood lipids, liver lipid accumulation, and liver injury markers were performed. The expression of G 0/G 1 switch gene 2(G0S2) and adipose triglyceride lipase (ATGL) was measured by qRT-PCR and Western blot, and gene expression was further verified using immunohistochemical staining. The effects of polydatin on HepG2 cell activity was assessed by CCK-8 assay, lipid accumulation was observed by oil red O staining, and the expression of G0S2 and ATGL was detected by qRT-PCR and Western blot. Results Polydatin significantly reduced the body weight, liver weight, and serum and liver tissue levels of aspartate aminotransferase (AST), alanine aminotransferase (ALT), triglyceride (TG), and total cholesterol (TC) in mice ( P<0.05), alleviated pathological liver damage, decreased G0S2 expression ( P<0.05), and increased ATGL expression ( P<0.05). At the cellular level, polydatin reduced lipid droplet accumulation, improved lipid metabolism, decreased G0S2 expression ( P<0.05), and increased ATGL expression ( P<0.05). Even in cells with knockdown of G0S2, polydatin still promoted fat decomposition ( P<0.01). Conclusion Polydatin promotes hepatic fat breakdown by regulating the expression of G0S2 and ATGL, helping to alleviate metabolic disorders and liver damage in the NAFLD mouse model caused by a high-fat diet, offering a new strategy for treating NAFLD.

Correlation between small intestinal bacterial overgrowth and cognitive function in peritoneal dialysis patients

Xu Hongting; Wang Liangjing; Li Dashan; Qi Xiangming

DOI: 专辑：医药卫生科技

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abstract:
Objective To explore the correlation between small intestinal bacterial overgrowth (SIBO) and cognitive impairment in patients undergoing peritoneal dialysis (PD). Methods60 PD patients and 46 non-dialysis patients with end-stage renal disease (ESRD) were included in this study. SIBO was detected by lactulose hydrogen methane breath test (LHMBT). The cognitive function levels of the subjects were evaluated using the Montreal cognitive assessment (MoCA) and mini-mental state examination (MMSE). The emotional states of the patients were assessed by self-rating anxiety scale (SAS) and self-rating depression scale (SDS). The gastrointestinal symptoms were evaluated using gastrointestinal symptom rating scale (GSRS). According to the results of LHMBT, the PD patients were further divided into two subgroups: SIBO-positive and SIBO-negative. The general conditions, laboratory data, and scores of each scale were compared between the two groups. Furthermore, according to the MoCA scores, the PD patients were divided into two groups: those with normal cognitive function and those with cognitive dysfunction. The positive rates of SIBO between the two groups were compared. Binary Logistic stepwise regression was used to explore whether SIBO was an independent risk factor for cognitive impairment in PD patients. At the same time, other independent influencing factors for cognitive impairment in PD patients were analyzed. Result s The positive rate of SIBO in PD patients was 40%. Among them, the positive rate of SIBO in the group with normal cognitive function during peritoneal dialysis was 27.27%, and the positive rate of SIBO in the group with cognitive dysfunction during peritoneal dialysis was 55.56%. There was a statistically significant difference in the positive rate of SIBO between the two groups ( P =0.026). Further analysis by multivariate Logistic stepwise regression showed that in addition to age ( OR=1.118, 95% CI 1.007-1.242, P =0.037), educational attainment（ OR=0.655，95% CI 0.442-0.972， P =0.036）, and hemoglobin （ OR=0.946，95% CI0.895-0.998， P =0.044）, SIBO （ OR=7.613，95% CI1.160-49.979， P =0.034）was also an independent risk factor for cognitive impairment in PD patients. ConclusionThe incidence of SIBO in PD patients is relatively high and is associated with multiple factors, among which SIBO may be closely related to cognitive dysfunction in PD patients.

Establishment of the EMT model of CoCl₂ -induced NRK-52E cells

Ni Lei; Sun Qingqing; Cheng Jiangrui; Wei Wei; Wang Chun

DOI: 专辑：医药卫生科技

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abstract:
Objective To establish an in vitrocell model of Cobalt dichloride (CoCl 2)-induced epithelial-mesenchymal transition (EMT) in rat renal tubular epithelial cells (NRK-52E). MethodsNRK-52E cells were cultured in vitroand randomly divided into a blank control group (NC group) and a CoCl 2 treatment group. The CoCl 2 treatment group underwent 1, 2, 3, and 4 cycles of treatment, with each cycle consisting of CoCl 2 treatment for 9 h followed by recovery in CoCl 2-free medium for 3 h. The optimal concentration and time of CoCl 2-induced EMT were screened using the CCK-8 assay. Morphological changes in cells were observed using light microscopy and phalloidin staining. The expression levels of EMT marker proteins were detected by Western blot and immunofluorescence. ResultsCompared with the NC group, stimulation by 100 μmol/L CoCl 2 for 48 h significantly induced apoptosis ( P<0.01), meeting the requirements for subsequent experiments. Western blot results showed that the expression of hypoxia-inducible factor-1α (HIF-1α) and α-smooth muscle actin (α-SMA) significantly increased in the 3-cycle group treated with 100 μmol/L CoCl 2 for 9 h followed by recovery for 3 h ( P<0.001), indicating the most pronounced fibrotic response. Observations under light microscopy and rhodamine-labeled phalloidin staining revealed that the morphological changes and cytoskeletal rearrangement of NRK-52E cells were most significant in the 3-cycle group treated with 100 μmol/L CoCl 2 for 9 h followed by recovery for 3 h, demonstrating the best model stability. Immunofluorescence results showed that compared with the NC group, the fluorescence intensity of the fibrous matrix protein Collagen I significantly increased in the 3-cycle group treated with 100 μmol/L CoCl 2 for 9 h followed by recovery for 3 h ( P<0.001). ConclusionThe protocol involves treating NRK-52E cells with 100 μmol/L CoCl₂ for 9 h, following 3 h of recovery in CoCl₂-free medium. Repeating this cycle three times can establish an in vitro EMT model.

Screening and validation of chemoresistance marker in lung adenocarcinoma based on gene expression profile

Wei Handong; Chen Shuxing; Liu Linting; Jing Zihan; Yang Yiting; Song Qiong; Wang Wenchu; Zou Chunlin; Wang Lihui

DOI:

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abstract:
ObjectiveTo discover molecular markers associated with lung adenocarcinoma diagnosis/prognosis and drug resistance through screening of differentially expressed genes based on published chip data in gene expression databases using bioinformatics methods. Methods Comprehensive analysis was performed in available mRNA microarray datasets including lung adenocarcinoma tissues dataset GSE32863 and lung adenocarcinoma taxane-platin resistance dataset GSE77209 from the gene expression omnibus (GEO) database. Gene ontology enrichment analysis, gene pathway enrichment analysis and protein interaction network analysis were performed based on significantly correlated genes. The expression level of genes was validated in the cancer genome atlas (TCGA) dataset. Survival differences were assessed by the log-rank test in TCGA lung adenocarcinoma dataset. Based on the publications genomics of drug sensitivity in cancer (GDSC) database in CellMiner cross database (CellMiner CDB), Pearson correlation analysis was used to analyze the correlation between differentially expressed genes and the half-maximal inhibitory concentration (IC 50) of anticancer drugs. ResultsThere were a total of 77 genes which had a different expression in resistance lung adenocarcinoma cells and lung adenocarcinoma cancer tissues. The functional enrichment analysis showed that these co-different expression genes were mainly enriched in microtubule, extracellular exosome, cell cycle and signaling by nuclear receptors. Protein–protein interactions (PPI) network screened 6 most connected genes as molecular complex (MCODE). Among the MCODE, overexpressed ubiquitin conjugating enzyme E2 T (UBE2T), kinesin family member 20A(KIF20A), PCNA clamp associated factor (KIAA0101), pituitary tumor-transforming gene 1 (PTTG1) and NIMA related kinase 2 (NEK2) were associated with poor outcomes. Survival analysis results showed that these five genes were upregulated in lung adenocarcinoma tissues and drug-resistant cells and were significantly associated with poor prognosis in lung adenocarcinoma patients. Drug sensitivity analysis results suggested that high expression of PTTG1 and UBE2T was significantly associated with sensitivity to multiple anticancer drugs, including paclitaxel and docetaxel. RT-PCR validation showed that PTTG1 and UBE2T were highly expressed in docetaxel-resistant cells A549-TXR and H358-TXR. ConclusionPTTG1 and UBE2T holds the potential to be chemoresistance markers in lung adenocarcinoma.

Porphyromonas gingivalispromotes esophageal squamous cell carcinoma progression and enhances cetuximab resistanceviaEGFR/GSK3β pathway induced EMT

Lang Yaowu; Chen Pan; Zhang Zichao; Liu Ke; Shi Linlin; Gao Shegan

DOI: 专辑：医药卫生科技

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abstract:
ObjectiveTo investigate the regulatory role of Porphyromonas gingivalis (Pg) infection on the EGFR/GSK3β signaling axis, and its impact on epithelial-mesenchymal transition (EMT) and cetuximab (Ctx) resistance in esophageal squamous cell carcinoma (ESCC). Methods Single cell RNA sequencing was employed to perform differential analysis of cellular subpopulations, identifying differentially expressed genes in ESCC tissues infected and non-infected with Pg. IHC was conducted to assess the expression of Pg and epidermal growth factor receptor (EGFR) in ESCC tissues. Western blot, RT-PCR, and IF staining were performed to evaluate EGFR expression in Pg infected ESCC cell lines KYSE70 and TE1. ESCC cells were treated with Pg and EGFR inhibitor Ctx, and divided into four groups: negative control (NC) group, P. gingivalis group, Ctx group, Pg+Ctx group. Cell proliferation, migration and invasion abilities were evaluated using CCK-8, plate cloning, wound healing and Transwell assay. Western blot analysis was performed to detect the expression of EMT and EGFR/GSK3β signaling pathway-associated proteins and their phosphorylation levels. Transforming growth factor-β1 (TGF-β1) was used to induce EMT in ESCC cells, promoting a transition from the epithelial phenotype to mesenchymal-like phenotype. The differential effects of Ctx on these two phenotypic states were subsequently compared. ResultsEpithelial cells were predominantly enriched in Pg-positive tissues, and Pg infection promoted the upregulation of EGFR expression in ESCC cells. Compared to the NC group, Pg treatment significantly enhanced the proliferation, invasion and migration capabilities of ESCC cells, and also increased chemoresistance to Ctx and reduced its antitumor efficacy. Pg induced EMT in ESCC cells via the EGFR/GSK3β signaling pathway. Notably, Ctx exhibited markedly weaker inhibitory effects on mesenchymal-like cells compared to epithelial ESCC cells. Conclusion Pg promotes ESCC cells proliferation, invasion and migration by regulating EMT through the EGFR/GSK3β signaling pathway, and enhances chemoresistance to Ctx.

Study on CTRP3-mediated UCHL1 enhancing SeVGMT reprogramming of CFs to protect cardiac function in MI mice

Song Yanbin; Zhang Yunqing; Liu Huiyu; Chen Junming

DOI: 专辑：医药卫生科技

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abstract:
Objective 　To investigate the effects of C1q tumor necrosis factor-related protein 3 (CTRP3)-enhanced Sendai virus (SeV) vector-overexpressing Gata4, Mef2c, and Tbx5 (SeVGMT) in the treatment of myocardial infarction (MI) mice and to analyze whether ubiquitin carboxyl-terminal hydrolase L1 (UCHL1) mediates this therapeutic pathway. Methods 　The mice were divided into 7 groups ( n=12): Sham group, MI group, SeVGMT group, CTRP3-Lv group, UCHL1-sh group, SeVGMT+CTRP3-Lv group, and SeVGMT+CTRP3-Lv+UCHL1-sh group. In the Sham group, only the skin was incised without ligation, while the coronary artery was ligated 2-3 mm below the left atrial appendage in mice in other groups. PBS was injected at three points in the myocardial infarction boundary in the Sham and MI groups 30 minutes after ligation. Mice in other groups were injected with SeVGMT, CTRP3-Lv, or UCHL1-sh according to their grouping. Four weeks after treatment, fractional shortening (FS), ejection fraction (EF), left ventricular end-diastolic diameter (LVIDd), left ventricular end-systolic diameter (LVIDs), heart rate (HR), mean arterial pressure (MAP), serum creatine kinase isoenzyme MB (CK-MB), myocardial troponin I (cTnI) and lactate dehydrogenase (LDH) levels, and myocardial tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β) and interleukin-6 (IL-6) levels in mice were detected. The pathological changes of myocardial tissue were detected by 2,3,5-triphenyltetrazolium chloride (TTC), hematoxylin-eosin (HE), Masson trichrome and terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) staining. The mRNA expressions of CTRP3 and UCHL1 were detected by qRT-PCR. The protein expressions of CTRP3, UCHL1, collagen Ⅰ, collagen Ⅲ, Bcl-2-associated X (Bax) and B-cell lymphoma/leukemia-2 (Bcl-2) in myocardial tissue were detected by Western blot or immunohistochemical staining. Results 　Compared with SeVGMT group and CTRP3-Lv group, the levels of EF, FS, HR and MAP in SeVGMT+CTRP3-Lv group increased ( P<0.05). The levels of LVIDd, LVIDs, CK-MB, cTnI, LDH, TNF-α, IL-1β and IL-6 decreased ( P<0.05). MI area, fibrosis area and TUNEL positive rate decreased ( P<0.05), the protein levels collagen Ⅰ, collagen Ⅲ and Bax decreased ( P<0.05), and Bcl-2 protein levels increased ( P<0.05). The mRNA and protein levels and relative staining intensity of CTRP3 and UCHL1 increased ( P<0.05). Compared with SeVGMT+CTRP3-Lv group, the addition of UCHL1-sh treatment (SeVGMT+CTRP3-Lv+UCHL1-sh group) significantly weakened the influence of SeVGMT+CTRP3-Lv on the above indexes ( P<0.05). Conclusion 　 CTRP3 mediated UCHL1 enhances the therapeutic effect of SeVGMT reprogrammed CFs on MI in mice.

Epidermal endoplasmic reticulum stress induced by UVB radiation and therapeutic interventions

Lin Boyang; Qiang Lei

DOI: 专辑：医药卫生科技

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