Purpose: To systematically analyze the disparity in uric acid reduction between losartan and other angiotensin receptor antagonists.Methods: A computer-based search was conducted in databases including EMBASE, PubMed, Wanfang, CNKI, Ovid MEDLINE, and Web of Science to identify original literature comparing the impact of losartan with other angiotensin receptor antagonists on blood uric acid levels. Utilizing the Cochrane Collaboration bias risk tool, a quality assessment of the included randomized controlled studies was conducted.Results: A total of 12 publications were obtained, consisting of 6 randomized controlled studies and 6 cohort studies. Five of the twelve publications assessed the impact of losartan compared to valsartan on blood uric acid levels. The heterogeneity analysis yielded I2 = 98 % (p < 0.01), indicating substantial variability among the studies. Findings indicated that losartan was more effective than valsartan in reducing blood uric acid levels (SMD = -3.26, 95 % CI (-5.01 to 1.51), p < 0.05). Four publications investigated the impact of losartan versus telmisartan on blood uric acid levels. The results revealed that losartan had a greater effect in reducing blood uric acid levels compared to telmisartan (SMD = -1.77, 95 % CI (-3.411 to -0.13), p < 0.05).Conclusion: Among the angiotensin receptor antagonists used as antihypertensive drugs, losartan stands out for its significant ability to reduce uric acid levels. This finding provides a strong evidencebase for making clinical medication decisions.
目的:系统分析氯沙坦与其他血管紧张素受体拮抗剂降低尿酸的差异。方法:计算机检索EMBASE、PubMed、万方、中国知网、Ovid MEDLINE、Web of Science等数据库，查找比较氯沙坦与其他血管紧张素受体拮抗剂对血尿酸水平影响的原始文献。利用Cochrane协作偏倚风险工具，对纳入的随机对照研究进行质量评估。结果:共获得文献12篇，其中随机对照研究6篇，队列研究6篇。12篇出版物中有5篇评估了氯沙坦与缬沙坦对血尿酸水平的影响。异质性分析得出I2 = 98% (p <0.01)，表明研究之间存在很大差异。结果表明，氯沙坦在降低血尿酸水平方面比缬沙坦更有效(SMD = -3.26, 95% CI (-5.01 ~ 1.51)， p <0.05)。四篇出版物调查了氯沙坦与替米沙坦对血尿酸水平的影响。结果显示，与替米沙坦相比，氯沙坦在降低血尿酸水平方面具有更大的效果(SMD = -1.77, 95% CI(-3.411至-0.13)，p <0.05)。结论:在血管紧张素受体拮抗剂中，氯沙坦具有显著的降低尿酸水平的作用。这一发现为临床用药决策提供了强有力的证据基础。
{"title":"Meta-analysis of the effect of losartan relative to other angiotensin receptor antagonists on serum uric acid level","authors":"Jinjie Zhou, Yongwei Zhang, Lin Cheng","doi":"10.4314/tjpr.v22i9.31","DOIUrl":"https://doi.org/10.4314/tjpr.v22i9.31","url":null,"abstract":"Purpose: To systematically analyze the disparity in uric acid reduction between losartan and other angiotensin receptor antagonists.Methods: A computer-based search was conducted in databases including EMBASE, PubMed, Wanfang, CNKI, Ovid MEDLINE, and Web of Science to identify original literature comparing the impact of losartan with other angiotensin receptor antagonists on blood uric acid levels. Utilizing the Cochrane Collaboration bias risk tool, a quality assessment of the included randomized controlled studies was conducted.Results: A total of 12 publications were obtained, consisting of 6 randomized controlled studies and 6 cohort studies. Five of the twelve publications assessed the impact of losartan compared to valsartan on blood uric acid levels. The heterogeneity analysis yielded I2 = 98 % (p < 0.01), indicating substantial variability among the studies. Findings indicated that losartan was more effective than valsartan in reducing blood uric acid levels (SMD = -3.26, 95 % CI (-5.01 to 1.51), p < 0.05). Four publications investigated the impact of losartan versus telmisartan on blood uric acid levels. The results revealed that losartan had a greater effect in reducing blood uric acid levels compared to telmisartan (SMD = -1.77, 95 % CI (-3.411 to -0.13), p < 0.05).Conclusion: Among the angiotensin receptor antagonists used as antihypertensive drugs, losartan stands out for its significant ability to reduce uric acid levels. This finding provides a strong evidencebase for making clinical medication decisions.","PeriodicalId":23347,"journal":{"name":"Tropical Journal of Pharmaceutical Research","volume":"1 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2023-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"135250946","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Qindan Du, Jiayao Chen, Honglei Li, Yixin Bian, Xiaoying Wang, Chen YQ, Xiaosong Ge
Purpose: To determine the role of Fragile X-related protein-1 (FXR1) in colon cancer progression and its relationship to patients’ survival.Methods: A total of 164 colorectal cancer (CRC) patients, admitted to the Affiliated Hospital of Jiangnan University, Wuxi, Jiangsu, China between 2006 and 2008, were included in this study. Immunohistochemistry was used to semi-quantitatively analyze the intensity and extent of immunological staining of diaminobenzidine-stained paraffin blocks of CRC samples. The study also retrieved COAD mRNA and patients’ clinical data from TCGA and cultured human colon cancer cell lines (SW480, SW620, HCT8, HCT116, and Caco2) in RPMI 1640 medium to assess the propensity of CRC cells to proliferate, invade the tumorigenicity in BALB/c nude mice.Results: The prognosis of CRC patients was inversely linked with the expression of FXR1. Additionally, FXR1 knockdown in CRC cells reduced cellular growth, colony development and tumorigenesis. After presenting BALB/c nude mice with tumors in FXR1 knockdown, the cells displayed higher E-cadherin levels (p < 0.01) as well as decreased TGF-1 (p < 0.01) and N-cadherin levels (p < 0.001).Conclusion: Fragile X-related protein-1 is an oncogene in colon cancer and its knockdown inhibits HCT116 cells from behaving malignantly. Thus, FXR1 is a potential treatment option for CRC.
{"title":"FXR1 knockdown inhibits the malignant behavior of colorectal cancer by suppressing epithelial-tomesenchymal transition","authors":"Qindan Du, Jiayao Chen, Honglei Li, Yixin Bian, Xiaoying Wang, Chen YQ, Xiaosong Ge","doi":"10.4314/tjpr.v22i9.1","DOIUrl":"https://doi.org/10.4314/tjpr.v22i9.1","url":null,"abstract":"Purpose: To determine the role of Fragile X-related protein-1 (FXR1) in colon cancer progression and its relationship to patients’ survival.Methods: A total of 164 colorectal cancer (CRC) patients, admitted to the Affiliated Hospital of Jiangnan University, Wuxi, Jiangsu, China between 2006 and 2008, were included in this study. Immunohistochemistry was used to semi-quantitatively analyze the intensity and extent of immunological staining of diaminobenzidine-stained paraffin blocks of CRC samples. The study also retrieved COAD mRNA and patients’ clinical data from TCGA and cultured human colon cancer cell lines (SW480, SW620, HCT8, HCT116, and Caco2) in RPMI 1640 medium to assess the propensity of CRC cells to proliferate, invade the tumorigenicity in BALB/c nude mice.Results: The prognosis of CRC patients was inversely linked with the expression of FXR1. Additionally, FXR1 knockdown in CRC cells reduced cellular growth, colony development and tumorigenesis. After presenting BALB/c nude mice with tumors in FXR1 knockdown, the cells displayed higher E-cadherin levels (p < 0.01) as well as decreased TGF-1 (p < 0.01) and N-cadherin levels (p < 0.001).Conclusion: Fragile X-related protein-1 is an oncogene in colon cancer and its knockdown inhibits HCT116 cells from behaving malignantly. Thus, FXR1 is a potential treatment option for CRC.","PeriodicalId":23347,"journal":{"name":"Tropical Journal of Pharmaceutical Research","volume":"8 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2023-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"135251665","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Purpose: To investigate the mechanism of liver cancer cell tolerance to the antiproliferative effect of transforming growth factor beta (TGF-β) based on miRNA levels.Methods: MiRNA microarray and quantitative reverse transcription-polymerase chain reaction (qRTPCR) were used to identify differentially expressed miRNAs in liver cancer Huh-7 cells treated with TGF-β. The effect of these miRNAs on patient survival was analyzed using Kaplan-Meier Plotter. Involvement of Smad2/Smad3 in TGF-β-induced miR-182 expression was determined using shRNA knockdown and qRT-PCR. Dose-dependent effect of TGF-β on miR-182 expression was investigated in Huh-7 cells and mouse primary liver cells using qRT-PCR. The effect of miR-182 on Huh-7 cell proliferation and apoptosis was studied using CFSE and Annexin V/PI assay. Direct targets of miR-182 in Huh-7 cells were identified using a luciferase reporter gene assay, while the influence of Recombinant Cell Adhesion Molecule 1 (CADM1) overexpression on Huh-7 cell proliferation and apoptosis treated with miR-182 was examined using lentivirus experiments, and CFSE and Annexin V/PI assays.Results: The expression levels of hsa-miR-181a, hsa-miR-182, hsa-miR-483, and hsa-miR-143 were significantly higher in serum samples from liver cancer patients (p < 0.05). Survival analysis showed that low expression of hsa-miR-182 and high expression of hsa-miR-483 increased the survival rate of liver cancer patients. Furthermore, TGF-β increased miR-182 expression in Huh-7 cells, but not in mouse primary liver cancer cells. The MiR-182 promoted Huh-7 cell proliferation and inhibited apoptosis. It targeted CADM1 mRNA 3'-UTR, decreasing CADM1 expression. Overexpression of MiR-182 significantly reduced cell proliferation and increased apoptosis in Huh-7 cells with CADM1 overexpression (p < 0.05).Conclusion: Transforming growth factor beta (TGF-β) facilitates the proliferation and repression of apoptosis of Huh-7 cells by increasing miR-182 expression and inhibiting CADMI expression.
{"title":"TGF-β promotes proliferation and inhibits apoptosis of liver cancer Huh-7 cells by regulating MiR-182/CADM1","authors":"An Wang, Yucheng Huang, Xiaoping Yang","doi":"10.4314/tjpr.v22i9.4","DOIUrl":"https://doi.org/10.4314/tjpr.v22i9.4","url":null,"abstract":"Purpose: To investigate the mechanism of liver cancer cell tolerance to the antiproliferative effect of transforming growth factor beta (TGF-β) based on miRNA levels.Methods: MiRNA microarray and quantitative reverse transcription-polymerase chain reaction (qRTPCR) were used to identify differentially expressed miRNAs in liver cancer Huh-7 cells treated with TGF-β. The effect of these miRNAs on patient survival was analyzed using Kaplan-Meier Plotter. Involvement of Smad2/Smad3 in TGF-β-induced miR-182 expression was determined using shRNA knockdown and qRT-PCR. Dose-dependent effect of TGF-β on miR-182 expression was investigated in Huh-7 cells and mouse primary liver cells using qRT-PCR. The effect of miR-182 on Huh-7 cell proliferation and apoptosis was studied using CFSE and Annexin V/PI assay. Direct targets of miR-182 in Huh-7 cells were identified using a luciferase reporter gene assay, while the influence of Recombinant Cell Adhesion Molecule 1 (CADM1) overexpression on Huh-7 cell proliferation and apoptosis treated with miR-182 was examined using lentivirus experiments, and CFSE and Annexin V/PI assays.Results: The expression levels of hsa-miR-181a, hsa-miR-182, hsa-miR-483, and hsa-miR-143 were significantly higher in serum samples from liver cancer patients (p < 0.05). Survival analysis showed that low expression of hsa-miR-182 and high expression of hsa-miR-483 increased the survival rate of liver cancer patients. Furthermore, TGF-β increased miR-182 expression in Huh-7 cells, but not in mouse primary liver cancer cells. The MiR-182 promoted Huh-7 cell proliferation and inhibited apoptosis. It targeted CADM1 mRNA 3'-UTR, decreasing CADM1 expression. Overexpression of MiR-182 significantly reduced cell proliferation and increased apoptosis in Huh-7 cells with CADM1 overexpression (p < 0.05).Conclusion: Transforming growth factor beta (TGF-β) facilitates the proliferation and repression of apoptosis of Huh-7 cells by increasing miR-182 expression and inhibiting CADMI expression.","PeriodicalId":23347,"journal":{"name":"Tropical Journal of Pharmaceutical Research","volume":"82 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2023-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"135251667","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Purpose: To evaluate the potential molecular mechanisms involved in refractory asthma in an animal model, and the potential therapeutic effect of MAPK1 knockdown on the disease.Methods: Eighteen female Institute of Cancer Research (ICR) mice, aged 8 - 10 weeks, were randomly divided into three groups: control, asthma model and refractory asthma, with 6 mice in each group. The expression of MAPK1 was knocked down in mice using an adenoviral vector. Subsequently, the methylation levels of MAPK1 promoter in mouse lung tissue were determined using methylation assays. Hematoxylin and eosin (H&E) staining and Periodic Acid-Schiff (PAS) staining were used to determine inflammatory and histological changes in lung tissues. Levels of immune cells were determined using flow cytometry, while Western blotting was used to measure the protein expression levels of ERK1/2, JNK, MEK1/2 and p38.Results: Methylation assay results show that mean methylation level of cg11335969 locus was significantly reduced in the refractory asthma mouse model (p < 0.05). The levels of IgG1 and IgM in refractory asthmatic mice were reduced after MAPK1 knockdown. There was a significantly reduced degree of lung lesions in mice (p < 0.05), as was reflected in effectively decreased histopathological changes. Protein levels of ERK1/2, JNK, MEK1/2 and p38, and the levels of neutrophils, dendritic cells, and macrophages were significantly decreased (p < 0.05).Conclusion: There is hypermethylated modification of MAPK1 at cg11335969 site in refractory asthma mouse model. Knockdown of MAPK1 attenuates inflammation and tissue damage, and reverses abnormal immune cell numbers in refractory asthma mice. Thus, MAPK1 inhibition may be a novel strategy for ameliorating immune abnormalities in refractory asthma.
{"title":"MAPK1 knockdown ameliorated immune and inflammatory abnormalities in a mouse model of refractory asthma","authors":"Shuang Lin, Xiaohong Yang","doi":"10.4314/tjpr.v22i9.9","DOIUrl":"https://doi.org/10.4314/tjpr.v22i9.9","url":null,"abstract":"Purpose: To evaluate the potential molecular mechanisms involved in refractory asthma in an animal model, and the potential therapeutic effect of MAPK1 knockdown on the disease.Methods: Eighteen female Institute of Cancer Research (ICR) mice, aged 8 - 10 weeks, were randomly divided into three groups: control, asthma model and refractory asthma, with 6 mice in each group. The expression of MAPK1 was knocked down in mice using an adenoviral vector. Subsequently, the methylation levels of MAPK1 promoter in mouse lung tissue were determined using methylation assays. Hematoxylin and eosin (H&E) staining and Periodic Acid-Schiff (PAS) staining were used to determine inflammatory and histological changes in lung tissues. Levels of immune cells were determined using flow cytometry, while Western blotting was used to measure the protein expression levels of ERK1/2, JNK, MEK1/2 and p38.Results: Methylation assay results show that mean methylation level of cg11335969 locus was significantly reduced in the refractory asthma mouse model (p < 0.05). The levels of IgG1 and IgM in refractory asthmatic mice were reduced after MAPK1 knockdown. There was a significantly reduced degree of lung lesions in mice (p < 0.05), as was reflected in effectively decreased histopathological changes. Protein levels of ERK1/2, JNK, MEK1/2 and p38, and the levels of neutrophils, dendritic cells, and macrophages were significantly decreased (p < 0.05).Conclusion: There is hypermethylated modification of MAPK1 at cg11335969 site in refractory asthma mouse model. Knockdown of MAPK1 attenuates inflammation and tissue damage, and reverses abnormal immune cell numbers in refractory asthma mice. Thus, MAPK1 inhibition may be a novel strategy for ameliorating immune abnormalities in refractory asthma.","PeriodicalId":23347,"journal":{"name":"Tropical Journal of Pharmaceutical Research","volume":"25 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2023-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"135251670","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Wanyan Yao, Jing Cai, Guanjun Liang, Mingding Li, Min Su
Purpose: To investigate the effect of Tiaoxie Yizhi Formula combined with atomoxetine and biofeedback therapy on the Swanson, Nolan, and Pelham-IV Rating Scale (SNAP-IV) score as well as Clinical Global Impression (CGI) score of school-age children with attention deficit hyperactivity disorder (ADHD).Methods: Clinical data of 85 school-age children with ADHD who were admitted to Dushu Lake Hospital from April 2019 to June 2022 were analyzed retrospectively. Patients treated with biofeedback therapy and atomoxetine for 1 month were defined as control group (n = 42), while those treated with Tiaoxie Yizhi Formula in addition to what was given control group were defined as study group (n = 43). Efficacy, Traditional Chinese Medicine (TCM) symptom scores, SNAP-IV score, CGI score and cerebral electrophysiological indices were compared between the groups. The scores of the main and secondary syndromes were also compared between two groups.Results: Treatment response rate in study group was significantly higher than in control group (p < 0.05). There was no significant difference in scores of the main syndromes and secondary syndromes, SNAP-IV score or CGI score between the two groups before treatment (p > 0.05). However, scores of the two groups decreased significantly after treatment, and study group had significantly lower scores than control group (p < 0.05). There was no significant difference in sensorimotor rhythms (SMR) waves, β waves, or θ waves between the two groups before and after treatment (p > 0.05).Conclusion: Tiaoxie Yizhi Formula plus atomoxetine plus biofeedback therapy improves ADHDsymptoms more tha n biofeedback therapy and atomoxetine combination as shown by the reduction in TCM, SNAP-IV and CGI scores. However, investigations will need to be carried out using a larger sample size in order to validate these findings.
{"title":"Effect of Tiaoxie Yizhi Formula combined with atomoxetine and biofeedback therapy of school-age children with attention deficit hyperactivity disorder","authors":"Wanyan Yao, Jing Cai, Guanjun Liang, Mingding Li, Min Su","doi":"10.4314/tjpr.v22i9.23","DOIUrl":"https://doi.org/10.4314/tjpr.v22i9.23","url":null,"abstract":"Purpose: To investigate the effect of Tiaoxie Yizhi Formula combined with atomoxetine and biofeedback therapy on the Swanson, Nolan, and Pelham-IV Rating Scale (SNAP-IV) score as well as Clinical Global Impression (CGI) score of school-age children with attention deficit hyperactivity disorder (ADHD).Methods: Clinical data of 85 school-age children with ADHD who were admitted to Dushu Lake Hospital from April 2019 to June 2022 were analyzed retrospectively. Patients treated with biofeedback therapy and atomoxetine for 1 month were defined as control group (n = 42), while those treated with Tiaoxie Yizhi Formula in addition to what was given control group were defined as study group (n = 43). Efficacy, Traditional Chinese Medicine (TCM) symptom scores, SNAP-IV score, CGI score and cerebral electrophysiological indices were compared between the groups. The scores of the main and secondary syndromes were also compared between two groups.Results: Treatment response rate in study group was significantly higher than in control group (p < 0.05). There was no significant difference in scores of the main syndromes and secondary syndromes, SNAP-IV score or CGI score between the two groups before treatment (p > 0.05). However, scores of the two groups decreased significantly after treatment, and study group had significantly lower scores than control group (p < 0.05). There was no significant difference in sensorimotor rhythms (SMR) waves, β waves, or θ waves between the two groups before and after treatment (p > 0.05).Conclusion: Tiaoxie Yizhi Formula plus atomoxetine plus biofeedback therapy improves ADHDsymptoms more tha n biofeedback therapy and atomoxetine combination as shown by the reduction in TCM, SNAP-IV and CGI scores. However, investigations will need to be carried out using a larger sample size in order to validate these findings.","PeriodicalId":23347,"journal":{"name":"Tropical Journal of Pharmaceutical Research","volume":"44 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2023-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"135251668","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Purpose: To investigate the correlation between breast cancer (BC), osteocalcin (OC) and hypertension risk in postmenopausal women.Methods: Two hundred patients with BC and 200 non–BC women who visited The First People's Hospital of Wenling Hospital, Wenling, China from June 2018 to March 2021 were included in the study. Fifty-three patients with hypertension and 157 non-hypertensive patients were included in the hypertension studies. The enrolled postmenopausal women were divided into control, BC, hypertensive and non–hypertensive groups and risk factors for hypertension were analyzed. Pearson's correlation coefficient was performed to correlate OC levels with clinical indices. The incidence of hypertension in each group was counted and its correlation with OC levels was determined using Chi–square test.Results: Age, BMI, OC, SBP, DBP, TC, TG, PTH and FPG levels were risk factors for the progression of hypertension in postmenopausal women (OR > 1, p < 0.05). Serum levels of OC in postmenopausal women had negative correlation with age, BMI, SBP, DBP, TC, TG, PTH, 25–(OH)D3 and FPG levels (r < 0, p < 0.05), but had positive correlation with HDL–C, CTX and PINP levels (r > 0, p < 0.05). With the elevation of OC levels, the incidence of hypertension showed a decreasing trend in postmenopausal women (p < 0.05).Conclusion: Menopause is a risk factor for BC in women, while low OC levels are significantly related to elevated risk of hypertension in postmenopausal women. These findings suggest that armacological intervention to increase OC levels may have potential benefits in mitigating the risk of hypertension in postmenopausal women.
目的:探讨绝经后妇女乳腺癌(BC)、骨钙素(OC)与高血压风险的关系。方法:2018年6月至2021年3月在中国温岭市温岭市第一人民医院就诊的200例BC患者和200例非BC女性纳入研究。53例高血压患者和157例非高血压患者被纳入高血压研究。将入选的绝经后妇女分为对照组、BC组、高血压组和非高血压组，分析高血压的危险因素。应用Pearson相关系数分析OC水平与临床指标的相关性。统计各组高血压发病率，并采用卡方检验确定其与OC水平的相关性。结果:年龄、BMI、OC、收缩压、舒张压、TC、TG、PTH和FPG水平是绝经后妇女高血压进展的危险因素(OR >1、p <0.05)。绝经后妇女血清OC水平与年龄、BMI、收缩压、舒张压、TC、TG、PTH、25 - (OH)D3、FPG水平呈负相关(r <0, p <0.05)，但与HDL-C、CTX、PINP水平呈正相关(r >0, p <0.05)。随着OC水平的升高，绝经后妇女高血压发病率呈下降趋势(p <0.05)。结论:绝经是女性BC的危险因素，而低OC水平与绝经后女性高血压风险升高显著相关。这些研究结果表明，提高OC水平的药理干预可能对减轻绝经后妇女高血压的风险有潜在的好处。
{"title":"Correlation between breast cancer and osteocalcin levels, and risk of hypertension in postmenopausal women: Implications for pharmacological intervention","authors":"Qianqian Cai, Mingyue Xu, Xueyan Zheng, Qiaoyun Zhu, Xiaodan Wu","doi":"10.4314/tjpr.v22i9.14","DOIUrl":"https://doi.org/10.4314/tjpr.v22i9.14","url":null,"abstract":"Purpose: To investigate the correlation between breast cancer (BC), osteocalcin (OC) and hypertension risk in postmenopausal women.Methods: Two hundred patients with BC and 200 non–BC women who visited The First People's Hospital of Wenling Hospital, Wenling, China from June 2018 to March 2021 were included in the study. Fifty-three patients with hypertension and 157 non-hypertensive patients were included in the hypertension studies. The enrolled postmenopausal women were divided into control, BC, hypertensive and non–hypertensive groups and risk factors for hypertension were analyzed. Pearson's correlation coefficient was performed to correlate OC levels with clinical indices. The incidence of hypertension in each group was counted and its correlation with OC levels was determined using Chi–square test.Results: Age, BMI, OC, SBP, DBP, TC, TG, PTH and FPG levels were risk factors for the progression of hypertension in postmenopausal women (OR > 1, p < 0.05). Serum levels of OC in postmenopausal women had negative correlation with age, BMI, SBP, DBP, TC, TG, PTH, 25–(OH)D3 and FPG levels (r < 0, p < 0.05), but had positive correlation with HDL–C, CTX and PINP levels (r > 0, p < 0.05). With the elevation of OC levels, the incidence of hypertension showed a decreasing trend in postmenopausal women (p < 0.05).Conclusion: Menopause is a risk factor for BC in women, while low OC levels are significantly related to elevated risk of hypertension in postmenopausal women. These findings suggest that armacological intervention to increase OC levels may have potential benefits in mitigating the risk of hypertension in postmenopausal women.","PeriodicalId":23347,"journal":{"name":"Tropical Journal of Pharmaceutical Research","volume":"17 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2023-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"135251669","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Purpose: To determine the correlation of serum TIMP-1 and sCD40L with peripheral neuropathy in type 2 diabetes (T2DM), and potential targets for pharmacological intervention.Methods: The study enrolled 97 subjects with T2DM. The 41 subjects with simple diabetes were classified as T2DM group, while 56 subjects with diabetic peripheral neuropathy (DPN) were included in the DPN group. A control group consisting of 50 healthy volunteers who conducted health checks during a similar time-period was also included. Clinical data and parameters were compared among the three groups, and TIMP-1 and sCD40L levels were determined. Univariate and multivariate logistic regression analyses were conducted to identify factors affecting DPN. The diagnostic value of TIMP-1 and sCD40L in DPN was also determined.Results: Body mass index (BMI) varied among the three groups (p < 0.05), but age or gender were not significantly different (p < 0.05). Duration of diabetes was longer in DPN group than in T2DM group (p < 0.05). The study also revealed statistically significant differences in fasting blood glucose (FBS), postprandial blood glucose, and glycosylated hemoglobin among the three groups. Tissue inhibitor of metalloproteinase-1 (TIMP-1) and soluble CD40 ligand (sCD40L) were important factors that affected the occurrence of diabetic peripheral neuropathy (p < 0.05).Conclusion: TIMP-1 and sCD40L levels reflect neurovascular injury in patients with diabetes, with potential as targets for pharmacological intervention for peripheral neuropathy. These findings espouse crucial clinical implications for early identification and treatment in type 2 diabetes.
{"title":"Relationship among serum TIMP-1, sCD40L and peripheral neuropathy in type 2 diabetes","authors":"Zhang Yong, Bai Feng","doi":"10.4314/tjpr.v22i9.24","DOIUrl":"https://doi.org/10.4314/tjpr.v22i9.24","url":null,"abstract":"Purpose: To determine the correlation of serum TIMP-1 and sCD40L with peripheral neuropathy in type 2 diabetes (T2DM), and potential targets for pharmacological intervention.Methods: The study enrolled 97 subjects with T2DM. The 41 subjects with simple diabetes were classified as T2DM group, while 56 subjects with diabetic peripheral neuropathy (DPN) were included in the DPN group. A control group consisting of 50 healthy volunteers who conducted health checks during a similar time-period was also included. Clinical data and parameters were compared among the three groups, and TIMP-1 and sCD40L levels were determined. Univariate and multivariate logistic regression analyses were conducted to identify factors affecting DPN. The diagnostic value of TIMP-1 and sCD40L in DPN was also determined.Results: Body mass index (BMI) varied among the three groups (p < 0.05), but age or gender were not significantly different (p < 0.05). Duration of diabetes was longer in DPN group than in T2DM group (p < 0.05). The study also revealed statistically significant differences in fasting blood glucose (FBS), postprandial blood glucose, and glycosylated hemoglobin among the three groups. Tissue inhibitor of metalloproteinase-1 (TIMP-1) and soluble CD40 ligand (sCD40L) were important factors that affected the occurrence of diabetic peripheral neuropathy (p < 0.05).Conclusion: TIMP-1 and sCD40L levels reflect neurovascular injury in patients with diabetes, with potential as targets for pharmacological intervention for peripheral neuropathy. These findings espouse crucial clinical implications for early identification and treatment in type 2 diabetes.","PeriodicalId":23347,"journal":{"name":"Tropical Journal of Pharmaceutical Research","volume":"33 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2023-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"135250939","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Cancer is one of the leading causes of death worldwide. The rising global death from cancer requires novel approaches for treating various types of cancer. Numerous malignancies are now being treated more effectively by immunotherapy. Dostarlimab is an example of an immune checkpoint inhibitor (ICI) that works by blocking the programmed cell death protein-1 receptor (PD-1). Dostarlimab has shifted the paradigm of treatment of cancer from using conventional therapies to a new, promising approach. This new approach increases the options of therapies and chances to achieve a higher response rate. Dostarlimab is a novel antibody, that prevents the binding of ligands to PD-1 on T-cells. Dostarlimab has demonstrated encouraging outcomes in the treatment of various cancers such as endometrial cancer, rectal cancer, and non–small cell lung cancer (NSCLC). The cure rate with dostarlimab in some types of cancer, such as rectal cancer, is 100 %. This review presents a recent understanding of the use of dostarlimab in clinical trials and opens up the doors for clinicians and investigators about future possibilities of using dostarlimab either alone or combined with other anticancer medications to treat various cancers.
{"title":"Dostarlimab: Novel paradigm shift in cancer therapy","authors":"Ali Alquraini","doi":"10.4314/tjpr.v22i9.32","DOIUrl":"https://doi.org/10.4314/tjpr.v22i9.32","url":null,"abstract":"Cancer is one of the leading causes of death worldwide. The rising global death from cancer requires novel approaches for treating various types of cancer. Numerous malignancies are now being treated more effectively by immunotherapy. Dostarlimab is an example of an immune checkpoint inhibitor (ICI) that works by blocking the programmed cell death protein-1 receptor (PD-1). Dostarlimab has shifted the paradigm of treatment of cancer from using conventional therapies to a new, promising approach. This new approach increases the options of therapies and chances to achieve a higher response rate. Dostarlimab is a novel antibody, that prevents the binding of ligands to PD-1 on T-cells. Dostarlimab has demonstrated encouraging outcomes in the treatment of various cancers such as endometrial cancer, rectal cancer, and non–small cell lung cancer (NSCLC). The cure rate with dostarlimab in some types of cancer, such as rectal cancer, is 100 %. This review presents a recent understanding of the use of dostarlimab in clinical trials and opens up the doors for clinicians and investigators about future possibilities of using dostarlimab either alone or combined with other anticancer medications to treat various cancers.","PeriodicalId":23347,"journal":{"name":"Tropical Journal of Pharmaceutical Research","volume":"4 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2023-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"135250947","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Sunbin Chen, Shibin Lin, Minghui Li, Siwei Li, Kefeng Yang
Purpose: To assess the efficacy of ultrasound-guided subacromial bursa (SAB) steroid injection for treating hemiplegic shoulder pain (HSP) after stroke (CS), as well as its impact on joint mobility, and inflammatory mediators.Methods: Seventy-two (72) patients with CS-related HSP were divided into two groups: study and control groups. The study group received ultrasound-guided SAB injection of triamcinolone acetonide in addition to conventional treatment, while control group received only conventional rehabilitation. Both groups received 4 weeks of treatment and were assessed using pain visual analogue scale (VAS) and passive range of motion (PROM) indices before treatment and at 1, 4, and 12 weeks after treatment. Additionally, the Fugl-Meyer motor function (FMA-U) scale score, activities of daily living (ADL) score, modified Barthel index (MBI), serum IL-1β, IL-6, nitric oxide (NO) levels, and incidence of adverse reactions were assessed before and after 4 weeks of treatment.Results: The study group had a significantly higher total efficacy/effectiveness (86.11 %) compared to control group (53.89 %). Both groups showed initial decreases and subsequent increases in VAS and PROM from week 1 to week 12 after treatment. However, the study group had significantly lower VAS scores, angle of forward flexion, abduction, and external rotation at all time points compared to control group (p < 0.05). At week 4, the study group had significantly higher FMA-U, ADL, and MBI scores, as well as significantly lower IL-1β, IL-6, and NO levels when compared to control group (p < 0.05).Conclusion: Ultrasound-guided SAB steroid injection improves the efficacy of HSP after CS, improves joint mobility, and reduces serum levels of IL-1β, IL-6, and NO. Further large-sample studies with increased sample sizes and longer investigation periods are needed to validate these findings.
{"title":"Efficacy of ultrasound-guided subacromial bursa steroid injection for treating shoulder pain in post-stroke hemiparetic patients","authors":"Sunbin Chen, Shibin Lin, Minghui Li, Siwei Li, Kefeng Yang","doi":"10.4314/tjpr.v22i9.15","DOIUrl":"https://doi.org/10.4314/tjpr.v22i9.15","url":null,"abstract":"Purpose: To assess the efficacy of ultrasound-guided subacromial bursa (SAB) steroid injection for treating hemiplegic shoulder pain (HSP) after stroke (CS), as well as its impact on joint mobility, and inflammatory mediators.Methods: Seventy-two (72) patients with CS-related HSP were divided into two groups: study and control groups. The study group received ultrasound-guided SAB injection of triamcinolone acetonide in addition to conventional treatment, while control group received only conventional rehabilitation. Both groups received 4 weeks of treatment and were assessed using pain visual analogue scale (VAS) and passive range of motion (PROM) indices before treatment and at 1, 4, and 12 weeks after treatment. Additionally, the Fugl-Meyer motor function (FMA-U) scale score, activities of daily living (ADL) score, modified Barthel index (MBI), serum IL-1β, IL-6, nitric oxide (NO) levels, and incidence of adverse reactions were assessed before and after 4 weeks of treatment.Results: The study group had a significantly higher total efficacy/effectiveness (86.11 %) compared to control group (53.89 %). Both groups showed initial decreases and subsequent increases in VAS and PROM from week 1 to week 12 after treatment. However, the study group had significantly lower VAS scores, angle of forward flexion, abduction, and external rotation at all time points compared to control group (p < 0.05). At week 4, the study group had significantly higher FMA-U, ADL, and MBI scores, as well as significantly lower IL-1β, IL-6, and NO levels when compared to control group (p < 0.05).Conclusion: Ultrasound-guided SAB steroid injection improves the efficacy of HSP after CS, improves joint mobility, and reduces serum levels of IL-1β, IL-6, and NO. Further large-sample studies with increased sample sizes and longer investigation periods are needed to validate these findings.","PeriodicalId":23347,"journal":{"name":"Tropical Journal of Pharmaceutical Research","volume":"58 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2023-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"135250949","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Purpose: To evaluate the effect of allogeneic platelet-rich plasma (PRP) on ulcer wound surface in streptozotocin-induced diabetic rats.Methods: A total of 20 male Sprague-Dawley (SD) rats were procured as skin ulcer as well as diabetes models, and randomly divided into control and PRP groups, respectively. Their wound surfaces were smeared with 0.9 % normal saline or an equal concentration of allogeneic PRP, respectively, and the pathological changes in the wound tissues were examined with the aid of hematoxylin-eosin (H&E) staining. Also, the expression levels of transforming growth factor-β1 (TGF-β1), matrix metalloproteinase-2 (MMP-2), and tissue inhibitor of metalloproteinase-2 (TIMP-2) in wound tissues were determined using enzyme-linked immunosorbent assay (ELISA).Results: Both purulent exudation and swelling of the wound surface were milder in the PRP group than in the control group, and the PRP group showed greater redness on the wound surface and more pronounced signs of epithelialization of the wound surface and its margins (p < 0.05). Wound healing rate in PRP group was higher than in the control group while the number of fibroblasts and new microvessels in the wound surface in the PRP group were greater than in the control group, accompanied by slighter inflammatory response compared to the control group. Furthermore, the PRP group expressed lower MMP-2, MMP-2/TIMP-2 ratio, and higher TGF-β1 and TIMP-2 levels than in the control group (p < 0.05).Conclusion: Allogeneic PRP treatment contributes to the healing of ulcer wound surface in diabetic rats, a process mediated by TGF-β1/MMP-2/TIMP-2 signaling pathway. Thus, PRP is a potential therapeutic agent for the management of diabetic ulcer wounds.
{"title":"Effect of allogeneic platelet-rich plasma on the healing of ulcer wound surface in streptozotocin-induced diabetic rats","authors":"Yueze Chen, Xiaowei Liu, Kesu Hu","doi":"10.4314/tjpr.v22i9.8","DOIUrl":"https://doi.org/10.4314/tjpr.v22i9.8","url":null,"abstract":"Purpose: To evaluate the effect of allogeneic platelet-rich plasma (PRP) on ulcer wound surface in streptozotocin-induced diabetic rats.Methods: A total of 20 male Sprague-Dawley (SD) rats were procured as skin ulcer as well as diabetes models, and randomly divided into control and PRP groups, respectively. Their wound surfaces were smeared with 0.9 % normal saline or an equal concentration of allogeneic PRP, respectively, and the pathological changes in the wound tissues were examined with the aid of hematoxylin-eosin (H&E) staining. Also, the expression levels of transforming growth factor-β1 (TGF-β1), matrix metalloproteinase-2 (MMP-2), and tissue inhibitor of metalloproteinase-2 (TIMP-2) in wound tissues were determined using enzyme-linked immunosorbent assay (ELISA).Results: Both purulent exudation and swelling of the wound surface were milder in the PRP group than in the control group, and the PRP group showed greater redness on the wound surface and more pronounced signs of epithelialization of the wound surface and its margins (p < 0.05). Wound healing rate in PRP group was higher than in the control group while the number of fibroblasts and new microvessels in the wound surface in the PRP group were greater than in the control group, accompanied by slighter inflammatory response compared to the control group. Furthermore, the PRP group expressed lower MMP-2, MMP-2/TIMP-2 ratio, and higher TGF-β1 and TIMP-2 levels than in the control group (p < 0.05).Conclusion: Allogeneic PRP treatment contributes to the healing of ulcer wound surface in diabetic rats, a process mediated by TGF-β1/MMP-2/TIMP-2 signaling pathway. Thus, PRP is a potential therapeutic agent for the management of diabetic ulcer wounds.","PeriodicalId":23347,"journal":{"name":"Tropical Journal of Pharmaceutical Research","volume":"18 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2023-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"135251530","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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