Analytical Cellular Pathology最新文献

{"title":"Chemoprevention of 4NQO-Induced Mouse Tongue Carcinogenesis by AKT Inhibitor through the MMP-9/RhoC Signaling Pathway and Autophagy.","authors":"Panpan Yin,&nbsp;Jiahui Chen,&nbsp;Yanlin Wu,&nbsp;Feng Gao,&nbsp;Jinlin Wen,&nbsp;Wenbin Zhang,&nbsp;Ying Su,&nbsp;Xinyan Zhang","doi":"10.1155/2022/3770715","DOIUrl":"https://doi.org/10.1155/2022/3770715","url":null,"abstract":"<p><p>Oral cancer (OC), the most common cancer in the head and neck, which has a poor prognosis, histopathologically follows a stepwise pattern of hyperplasia, dysplasia, and cancer. Blocking the progression of OC in the precancer stage could greatly improve the survival and cure rates. AKT protein plays a critical role in the signal transduction of cancer cells, and we found that AKT was overexpressed in human OC samples through analysis of TCGA database. Therefore, this study is aimed at investigating the chemopreventive effect of an AKT inhibitor (MK2206 2HCl) on OC. <i>In vivo</i>, we established a 4-nitroquinoline-1-oxide- (4NQO-) induced mouse tongue carcinogenesis model to investigate the potential chemopreventive effect of MK2206 2HCl on mouse OC resulting from 4NQO. The results showed that MK2206 2HCl could significantly reduce the incidence rate and growth of OC, inhibit the transformation of dysplasia to cancer in the 4NQO-induced mouse tongue carcinogenesis model, and simultaneously markedly suppress cell proliferation, angiogenesis, and mast cell (MC) infiltration in 4NQO-induced mouse tongue cancers. <i>In vitro</i>, our results revealed that MK2206 2HCl could also inhibit oral squamous cell carcinoma (OSCC) cell malignant biological behaviors, including cell proliferation, colony formation, cell invasion, and migration, while promoting apoptosis. Mechanistic studies revealed that MK2206 2HCl suppressed matrix metalloproteinase 9 (MMP-9) and RhoC expression and promoted autophagy gene LC3 II expression. In summary, our findings demonstrated the chemopreventive effect of MK2206 2HCl on the 4NQO-induced mouse tongue carcinogenesis model, which likely has an underlying mechanism mediated by the MMP-9/RhoC signaling pathway and autophagy.</p>","PeriodicalId":49326,"journal":{"name":"Analytical Cellular Pathology","volume":null,"pages":null},"PeriodicalIF":3.2,"publicationDate":"2022-10-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9556259/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"33514883","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"YAP Overexpression in Breast Cancer Cells Promotes Angiogenesis through Activating YAP Signaling in Vascular Endothelial Cells.","authors":"Yu Yan,&nbsp;Qiang Song,&nbsp;Li Yao,&nbsp;Liang Zhao,&nbsp;Hui Cai","doi":"10.1155/2022/5942379","DOIUrl":"https://doi.org/10.1155/2022/5942379","url":null,"abstract":"<p><strong>Purpose: </strong>The YAP signaling pathway is altered and implicated as oncogenic in human mammary cancers. However, roles of YAP signaling that regulate the breast tumor angiogenesis have remained elusive. Tumor angiogenesis is coordinated by the activation of both cancer cells and vascular endothelial cells. Whether the YAP signaling pathway can regulate the intercellular interaction between cancer cells and endothelial cells is essentially unknown.</p><p><strong>Methods: </strong>The effects of YAP on tumor angiogenesis, migration, and proliferation of vascular endothelial cells were evaluated in vitro. Expression of proteins and phosphorylating proteins involved in YAP, G13-RhoA, and PI3K/Akt signaling pathways was evaluated using the Western blotting, immunofluorescence staining, and immunohistochemistry analysis. In addition, the effects of YAP on breast cancer angiogenesis were evaluated in vivo by tumor xenograft mice.</p><p><strong>Results: </strong>We showed here that conditioned media from YAP overexpressed breast cancer cells (CM-YAP+) could promote angiogenesis, accompanied by increased tube formation, migration, and proliferation of human umbilical vein endothelial cells (HUVECs). Down regulation of YAP in HUVECs reversed CM-YAP+ induced angiogenesis. CM-YAP+ time-dependently activated YAP in HUVECs by dephosphorylating YAP and increasing nuclear translocation. We also identified that both G₁₃-RhoA and PI3K/Akt signaling pathway were necessary for CM-YAP+ induced activation of YAP. Besides, connective tissue growth factor (CTGF) and angiopoietin-2 (ANG-2) acted as down-stream of YAP in HUVECs to promote angiogenesis. In addition, subcutaneous tumors nude mice model demonstrated that tumors overexpressed YAP revealed more neovascularization in vivo.</p><p><strong>Conclusion: </strong>YAP-YAP interaction between breast cancer cells and endothelial cells could promote tumor angiogenesis, supporting that YAP is a potential marker and target for developing novel therapeutic strategies against breast cancer.</p>","PeriodicalId":49326,"journal":{"name":"Analytical Cellular Pathology","volume":null,"pages":null},"PeriodicalIF":3.2,"publicationDate":"2022-10-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9550503/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"33502846","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Tetrandrine Attenuates Podocyte Injury by Inhibiting TRPC6-Mediated RhoA/ROCK1 Pathway.","authors":"Lichan Mao, Yin Ding, Dongrong Yu, Jiazhen Yin, Jin Yu","doi":"10.1155/2022/7534181","DOIUrl":"10.1155/2022/7534181","url":null,"abstract":"<p><p>Tetrandrine (Tet), a compound found in a traditional Chinese medicine, presents the protective effect for kidney function. Our study is aimed at clarifying the efficacy and underlying mechanism of Tet on podocyte injury. In this study, podocyte injury was induced in rats with adriamycin (ADR), and MPC5 podocytes were constructed with TRPC6 overexpression. We found that Tet treatment reduced the levels of proteinuria, serum creatinine, and blood urea nitrogen and increased plasma albumin levels in ADR-induced rats. Tet reduced intracellular Ca²⁺ influx and apoptosis in MPC5 podocytes overexpressing TRPC6. Tet downregulated the expression of renal TRPC6, RhoA, and ROCK1 and upregulated the expression of synaptopodin; meanwhile, it reduced calcineurin activity <i>in vivo</i> and <i>in vitro</i>. In conclusion, Tet protects against podocyte by affecting TRPC6 and its downstream RhoA/ROCK1 signaling pathway.</p>","PeriodicalId":49326,"journal":{"name":"Analytical Cellular Pathology","volume":null,"pages":null},"PeriodicalIF":2.6,"publicationDate":"2022-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9553700/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"33516943","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Transgelin-2 Involves in the Apoptosis of Colorectal Cancer Cells Induced by Tanshinone-IIA.","authors":"Yingru Zhang,&nbsp;Yiyang Zhao,&nbsp;Jingwen Liu,&nbsp;Chunpu Li,&nbsp;Ying Feng,&nbsp;Shasha Jiang,&nbsp;Xiaoting Sun,&nbsp;Xueqing Hu,&nbsp;Yan Wang","doi":"10.1155/2022/9358583","DOIUrl":"https://doi.org/10.1155/2022/9358583","url":null,"abstract":"<p><p>Tanshinone IIA (TanIIA) is the main active ingredient in the fat-soluble components isolated from <i>Salvia miltiorrhiza</i> Bunge. Our previous studies have convincingly proved that TanIIA is an effective drug against human colorectal carcinoma cells. In order to further demonstrate the effect of TanIIA on CRC, we carried out exploratory research about it in vivo and in vitro. The results demonstrated that TanIIA were observably more effective than control group in preventing tumor growth, and it has increased the survival time. Cancer cells viability and proliferation were accompanied by concentration and time dependent decline reached with TanIIA. We found that TanIIA altered the morphology of cytoskeleton and it could obviously induce apoptosis of colorectal cancer cells and block the cells in the G0/G1 phase. TanIIA also increased phosphorylation of p38MAPK, upregulated ATF-2 expression and downregulated Transgelin-2 expression, which could be reversed by SB203580, a p38MAPK-specific inhibitor. Our results suggested that TanIIA could induce apoptosis of colorectal cancer and block the cells in G0/G1 phase involved in downregulating the expression of Transgelin-2 through p38MAPK signal pathway.</p>","PeriodicalId":49326,"journal":{"name":"Analytical Cellular Pathology","volume":null,"pages":null},"PeriodicalIF":3.2,"publicationDate":"2022-09-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9532164/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"33492207","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Prediction of Necroptosis-Related lncRNAs in Prognosis and Anticancer Therapy of Colorectal Cancer.","authors":"Hanyu Xiao,&nbsp;Qidan Pang,&nbsp;Yong Wang,&nbsp;Suhe Lai,&nbsp;Hong Chen","doi":"10.1155/2022/7158684","DOIUrl":"https://doi.org/10.1155/2022/7158684","url":null,"abstract":"<p><strong>Background: </strong>Colorectal cancer is one of the most common gastrointestinal malignancies globally. Necroptosis has been proved to play a role in the occurrence and development of the tumor, which makes it a new target for molecular therapy. However, the role of necroptosis in colorectal cancer remains unknown yet. Our study aims to build a prognostic signature of necroptosis-related lncRNAs (nrlncRNAs) to predict the outcomes of patients with colorectal cancer and facilitate in anticancer therapy.</p><p><strong>Method: </strong>We obtained RNA-seq and clinical data of colorectal adenocarcinoma from the TCGA database and got prognosis-related nrlncRNAs by univariate regression analysis. Then, we carried out the LASSO regression and multivariate regression analysis to build the prognostic signature, whose predictive ability was tested by the Kaplan-Meier as well as ROC curves and verified by the internal cohort. Moreover, we divided the cohort into 2 groups based on median of risk scores: high- and low-risk groups. By analyzing the difference in the tumor microenvironment, microsatellite instability, and tumor mutation burden between the two groups, we explored the potential chemotherapy and immunotherapy drugs.</p><p><strong>Results: </strong>We screened out 9 nrlncRNAs and built a prognostic signature based on them. With its good prognostic ability, the risk scores can act as an independent prognostic factor for patients with colorectal cancer. The overall survival rate of patients in high-risk group was significantly higher than the low-risk one. Furthermore, risk scores can also give us hints about the tumor microenvironment and facilitate in predicting the response to the CTLA-4 blocker treatment and other chemotherapeutic agents with potential efficacy such as cisplatin and staurosporine.</p><p><strong>Conclusions: </strong>In conclusion, our prognostic signature of necroptosis-related lncRNAs can facilitate in predicting the prognosis and response to the anticancer therapy of colorectal cancer patients.</p>","PeriodicalId":49326,"journal":{"name":"Analytical Cellular Pathology","volume":null,"pages":null},"PeriodicalIF":3.2,"publicationDate":"2022-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9527116/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"33489866","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"TAZ Regulates the Cisplatin Resistance of Epithelial Ovarian Cancer Cells via the ANGPTL4/SOX2 Axis.","authors":"Caihong Li,&nbsp;Qin Wang,&nbsp;Youzhen Luo,&nbsp;Juan Xiang","doi":"10.1155/2022/5632164","DOIUrl":"https://doi.org/10.1155/2022/5632164","url":null,"abstract":"<p><strong>Objective: </strong>Epithelial ovarian cancer (EOC) is a fatal gynecological malignancy. This study explored the mechanism of TAZ in regulating drug sensitivity of cisplatin (DDP-)-resistant EOC cells through the ANGPTL4/SOX2 axis.</p><p><strong>Methods: </strong>The A2780/DDP cells were prepared by stepwise progressive concentration method. The drug resistance and TAZ expression in EOC cells were determined. Drug sensitivity was measured after TAZ overexpression in A2780 cells and TAZ downregulation in A2780/DDP cells, respectively. The effects of TAZ knockdown on apoptosis rate, stemness, and cancer stem cell (CSC) marker (CD44, OCT4, and ALDH1A) levels in A2780/DDP and DDP-treated A2780/DDP cells were assessed. The binding of TAZ and ANGPTL4 was verified using ChIP-qPCR, and ANGPTL4 and SOX2 levels were determined. The effects of different combined treatments of TAZ, ANGPTL4, and SOX2 on drug sensitivity of A2780/DDP cells and DDP-treated A2780/DDP cells were evaluated.</p><p><strong>Results: </strong>TAZ was upregulated in drug-resistant EOC cells. TAZ knockdown significantly increased the drug sensitivity of A2780/DDP cells, while TAZ overexpression markedly decreased the drug sensitivity of A2780 cells. TAZ silencing promoted apoptosis of drug-resistant EOC cells and inhibited cell stemness. TAZ targeted ANGPTL4 and TAZ silencing enhanced drug sensitivity of A2780/DDP cells by inhibiting ANGPTL4. ANGPTL4 overexpression elevated SOX2 expression, and SOX2 downregulation reduced the drug resistance and promoted the apoptosis of A2780/DDP cells.</p><p><strong>Conclusion: </strong>TAZ regulates DDP sensitivity of drug-resistant EOC cells via the ANGPTL4/SOX2 axis.</p>","PeriodicalId":49326,"journal":{"name":"Analytical Cellular Pathology","volume":null,"pages":null},"PeriodicalIF":3.2,"publicationDate":"2022-09-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9553699/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"33514885","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Comprehensive Analysis of the Role of <i>SLC2A3</i> on Prognosis and Immune Infiltration in Head and Neck Squamous Cell Carcinoma.","authors":"Manru Chu,&nbsp;Ke Zheng,&nbsp;Xiaojie Li,&nbsp;Zhiqiang Luo,&nbsp;Xin Yang,&nbsp;Changbo Wei","doi":"10.1155/2022/2371057","DOIUrl":"https://doi.org/10.1155/2022/2371057","url":null,"abstract":"<p><strong>Background: </strong><i>SLC2A3</i> is upregulated in various cancer types and promotes proliferation, invasion, and metabolism. However, its role in the prognosis and immune regulation of head and neck squamous cell carcinoma (HNSCC) is still obscure. This study is aimed at exploring the prognostic and immunotherapeutic potential of <i>SLC2A3</i> in HNSCC.</p><p><strong>Methods: </strong>All data were downloaded from TCGA database and integrated via R software. <i>SLC2A3</i> expression was evaluated using R software, TIMER, CPTAC, and HPA databases. The association between <i>SLC2A3</i> expression and clinicopathologic characteristics was assessed by R software. The effect of <i>SLC2A3</i> on survival was analyzed by R software and Kaplan-Meier Plotter. Genomic alterations in <i>SLC2A3</i> were investigated using the cBioPortal database. Coexpression of <i>SLC2A3</i> was studied using LinkedOmics and STRING, and enrichment analyses were performed with R software. The relationship between <i>SLC2A3</i> expression and immune infiltration was determined using TIMER and TISIDB databases. Immune checkpoints and ESTIMATE score were analyzed via the SangerBox database.</p><p><strong>Results: </strong><i>SLC2A3</i> expression was upregulated in HNSCC tissues compared to normal tissues. It was significantly related to TNM stage, histological grade, and alcohol history. High <i>SLC2A3</i> expression was associated with poor prognosis in HNSCC. Coexpression analysis indicated that <i>SLC2A3</i> mostly participated in the HIF-1 signaling pathway and glycolysis. Furthermore, <i>SLC2A3</i> expression strongly correlated with tumor-infiltrating lymphocytes in HNSCC.</p><p><strong>Conclusion: </strong><i>SLC2A3</i> could serve as a potential prognostic biomarker for tumor immune infiltration in HNSCC.</p>","PeriodicalId":49326,"journal":{"name":"Analytical Cellular Pathology","volume":null,"pages":null},"PeriodicalIF":3.2,"publicationDate":"2022-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9553684/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"33514886","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Prognostic Value of GPNMB, EGFR, p-PI3K, and Ki-67 in Patients with Esophageal Squamous Cell Carcinoma.","authors":"Bo Wang,&nbsp;Mengyan Li,&nbsp;Anna Su,&nbsp;Yongmei Gao,&nbsp;Yan Shi,&nbsp;Chao Li,&nbsp;Wenying Liu,&nbsp;Liping Su,&nbsp;Wan Li,&nbsp;Yuqing Ma","doi":"10.1155/2022/9303081","DOIUrl":"https://doi.org/10.1155/2022/9303081","url":null,"abstract":"<p><strong>Background: </strong>GPNMB is a newly discovered tumour-promoting factor that may promote tumour cell progression by activating the PI3K/AKT pathway by EGFR. However, there are insufficient studies about GPNMB in ESCC. This study investigated the relationship between GPNMB and EGFR/PI3K pathway genes in ESCC.</p><p><strong>Methods: </strong>The expression levels of GPNMB, EGFR, p-PI3K, and Ki-67 were examined using immunohistochemistry. Statistical analysis was done by SPSS 22.0 and R.</p><p><strong>Results: </strong>GPNMB mRNA expression is higher in ESCC compared with paracancerous tissues. The expression of EGFR, PIK3CA, PIK3CB, and AKT1 was increased in GPNMB upregulated samples. GPNMB expression was positively correlated with EGFR, p-PI3K, and Ki-67 expression. GPNMB was expressed higher in the AJCC III stage, lymph node metastasis, and moderately poorly differentiated patients. EGFR was higher expressed in patients with vascular invasion; p-PI3K expression in Kazak was higher than that in Han; Ki-67 expression was higher in tumour size ≥ 3 cm. Patients with high expression of GPNMB, p-PI3K, and Ki-67 had worse OS. p-PI3K, Ki-67, nerve invasion, and lymphatic metastasis were independent risk factors, and postoperative adjuvant therapy was a protective factor in ESCC.</p><p><strong>Conclusion: </strong>As a tumour-promoting factor, GPNMB is expected to be a potential target for ESCC.</p>","PeriodicalId":49326,"journal":{"name":"Analytical Cellular Pathology","volume":null,"pages":null},"PeriodicalIF":3.2,"publicationDate":"2022-08-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9452951/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"33459136","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"circ_0052184 Promotes Colorectal Cancer Progression via Targeting miR-604/HOXA9 Axis.","authors":"Yandong Huang, Qinyang Bai, Zhanlong Wang, Hongbo Yu, Yanru Li, Hao Lu, Huimin Kang, Xuewei Shi, Kai Feng","doi":"10.1155/2022/8583382","DOIUrl":"10.1155/2022/8583382","url":null,"abstract":"<p><strong>Background: </strong>The mortality rate of colorectal cancer (CRC) ranks second. circRNAs are abnormal expression in some diseases, and their dysregulation is associated with cancer progression. Recent studies have shown that the malignant progression of colorectal cancer is inseparable from the abnormal expression of circRNAs.</p><p><strong>Methods: </strong>First, the circ_0052184 expression in clinical tissue and cell samples was analyzed by qRT-PCR. Then, we constructed circ_0052184-silenced CRC cells and detected by qRT-PCR. Furthermore, the proliferation ability of cells was detected by colony formation assay. Cell migration ability was tested by wound healing assay and transwell assay. Cell invasion ability was detected by transwell assay.</p><p><strong>Results: </strong>Expression of circ_0052184 was significantly increased in colorectal cancer cell lines and tissues. Silencing circ_0052184 affected the proliferation, migration, and invasion of colorectal cancer cells. miR-604 was targeted by circ_0052184. The downstream target of miR-604 was HOXA9, and silencing circ_0052184 inhibited HOXA9 expression. The existence of the circ_0052184/miR-604/HOXA9 regulatory network in colorectal cancer was validated. circ_0052184 promoted the occurrence and development of colorectal cancer by targeting the miR-604/HOXA9 axis.</p><p><strong>Conclusions: </strong>Our study revealed that the molecular mechanism of circ_0052184 regulated the miR-604/HOXA9 axis, which might promote the malignant progression of colorectal cancer cells.</p>","PeriodicalId":49326,"journal":{"name":"Analytical Cellular Pathology","volume":null,"pages":null},"PeriodicalIF":2.6,"publicationDate":"2022-08-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9440801/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40352294","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Valsartan in Combination with Tripterygium Glycosides Protects against Chronic Nephritis via the Toll-Like Receptor 4 Pathway.","authors":"Jiabao Dong,&nbsp;Duo Huang,&nbsp;Ling Jing,&nbsp;Mengmeng Wu","doi":"10.1155/2022/4807028","DOIUrl":"https://doi.org/10.1155/2022/4807028","url":null,"abstract":"<p><strong>Objective: </strong>Valsartan has been studied to exert effects on kidney disease. However, the concrete function of valsartan in combination with tripterygium glycosides in chronic nephritis remained largely unknown. The study was designed to unravel the impacts of valsartan and tripterygium glycosides in chronic nephritis through the Toll-like Receptor 4 (TLR4) pathway.</p><p><strong>Methods: </strong>The renal function indicators such as serum creatinine (Scr), blood urea nitrogen (BUN) and <i>β</i>2 microglobulin (<i>β</i>2-MG), 24 h urine protein <b>(</b>Upro) levels, and blood lipid indicators such as total cholesterol (TC), low-density lipoprotein (LDL-C), triacylglycerol (TG) and high-density lipoprotein (HDL-C), inflammatory factors (e.g., IL-1<i>β</i> and IL-8), and the proportion of T lymphocyte subpopulations (CD4+ and CD8+) were detected in chronic nephritis patients before and after treatment with valsartan alone or valsartan combined with tripterygium glycosides. Symptoms of adverse reactions were recorded. TLR4 expression in the patients' serum was examined.</p><p><strong>Results: </strong>Compared to patients before treatment, after treatment with valsartan alone or valsartan combined with tripterygium glycosides, the renal function indicators Scr, BUN, and 24 h levels were reduced, and TC, TG, and LDL-C levels were reduced, while HDL-C levels were elevated; inflammatory responses (IL-1<i>β</i> and IL-8) were mitigated; CD4+ ratio and CD4+/CD8+ ratio increased yet CD8+ ratio decreased; TLR4 expression was silenced after treatment. All of the changes were more obvious in patients after being treated with valsartan combined with tripterygium glycosides.</p><p><strong>Conclusion: </strong>Valsartan in combination with tripterygium glycosides protects against chronic nephritis via suppressing the Toll-like Receptor 4 pathway.</p>","PeriodicalId":49326,"journal":{"name":"Analytical Cellular Pathology","volume":null,"pages":null},"PeriodicalIF":3.2,"publicationDate":"2022-08-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9433283/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40349018","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}