The Kaohsiung journal of medical sciences最新文献

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Chinese translation validation of the adherence barrier questionnaire (intravitreal anti-vascular endothelial growth factor therapy) in Taiwan. 视网膜内抗血管内皮生长因子治疗)依从性障碍问卷的中文翻译在台湾的验证。
The Kaohsiung journal of medical sciences Pub Date : 2024-12-01 Epub Date: 2024-11-14 DOI: 10.1002/kjm2.12905
Yi-Chun Chi, Hui-Min Hsieh, Sabrina Müller, Shwu-Jiuan Sheu
{"title":"Chinese translation validation of the adherence barrier questionnaire (intravitreal anti-vascular endothelial growth factor therapy) in Taiwan.","authors":"Yi-Chun Chi, Hui-Min Hsieh, Sabrina Müller, Shwu-Jiuan Sheu","doi":"10.1002/kjm2.12905","DOIUrl":"10.1002/kjm2.12905","url":null,"abstract":"","PeriodicalId":94244,"journal":{"name":"The Kaohsiung journal of medical sciences","volume":" ","pages":"1121-1122"},"PeriodicalIF":0.0,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11618488/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142635630","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Effects of insulin glargine U300 versus insulin degludec U100 on glycemic variability, hypoglycemia, and diet evaluated by continuous glucose monitoring in type 1 diabetes: a retrospective cross-sectional study. 胰岛素格列卫 U300 与胰岛素德格列奈 U100 对 1 型糖尿病患者血糖变异性、低血糖和饮食的影响:一项回顾性横断面研究。
The Kaohsiung journal of medical sciences Pub Date : 2024-12-01 Epub Date: 2024-11-26 DOI: 10.1002/kjm2.12909
Pin-Lun Tsai, Chia-Hung Lin, Yu-Yao Huang, Hsin-Yun Chen, Yi-Hsuan Lin
{"title":"Effects of insulin glargine U300 versus insulin degludec U100 on glycemic variability, hypoglycemia, and diet evaluated by continuous glucose monitoring in type 1 diabetes: a retrospective cross-sectional study.","authors":"Pin-Lun Tsai, Chia-Hung Lin, Yu-Yao Huang, Hsin-Yun Chen, Yi-Hsuan Lin","doi":"10.1002/kjm2.12909","DOIUrl":"10.1002/kjm2.12909","url":null,"abstract":"<p><p>The impacts of insulin degludec U100 (Deg-100) and insulin glargine U300 (Gla-300) on glycemic variability (GV) in patients with type 1 diabetes, as well as the impact of major nutrient components on GV in these patients, remain unclear. This was an observational, cross-sectional, retrospective study. Type 1 diabetes mellitus patients treated with either Deg-100 or Gla-300 as basal insulin were enrolled. After the participants underwent continuous glucose monitoring, GV indices and major nutrient components were analyzed. Forty patients with type 1 diabetes were enrolled, and 20 participants used Deg-100, and 20 used Gla-300. There was no significant difference in major nutrient components between the two groups. Better GV indices of standard deviation, coefficient of variation, mean amplitude of glycemic excursion, AUC<sub>n</sub>, M-value, CONGA1, CONGA2, and CONGA4 were noted in the Gla-300 group versus Deg-100 group. Compared with patients who received once-daily injection in the morning (QD), Deg-100 administration once daily at bedtime (HS) yielded a higher low blood glucose index during both day and nocturnal periods, indicating a higher risk of hypoglycemic events. By contrast, there were significantly lower levels of CONGA1, CONGA2, and CONGA4 during insulin Gla-300 QD administration than during HS administration, indicating a lower GV of a short interval. In this real-world study involving type 1 diabetes patients, Gla-300 appears to offer more stable glucose variability than Deg-100. Administering once-daily injections could lower the risk of hypoglycemia in the Deg-100 group and minimize GV in the Gla-300 group compared to bedtime injections.</p>","PeriodicalId":94244,"journal":{"name":"The Kaohsiung journal of medical sciences","volume":" ","pages":"1086-1094"},"PeriodicalIF":0.0,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11618557/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142718030","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Metabolic syndrome and spatial disparities: The role of socioeconomic deprivation and medical resource availability in the Cijin district, Taiwan. 代谢综合征与空间差异:台湾慈济地区社会经济贫困和医疗资源可用性的作用。
The Kaohsiung journal of medical sciences Pub Date : 2024-12-01 Epub Date: 2024-11-14 DOI: 10.1002/kjm2.12908
Pei-Hung Su, Jong-Rung Tsai, Wei-Lun Chang, Hui-Min Hsieh
{"title":"Metabolic syndrome and spatial disparities: The role of socioeconomic deprivation and medical resource availability in the Cijin district, Taiwan.","authors":"Pei-Hung Su, Jong-Rung Tsai, Wei-Lun Chang, Hui-Min Hsieh","doi":"10.1002/kjm2.12908","DOIUrl":"10.1002/kjm2.12908","url":null,"abstract":"<p><p>Metabolic syndrome (MetS) is a global health concern with spatial disparities, especially in disadvantaged neighborhoods. This study aimed to examine the association between area-level socioeconomic deprivation, the availability of medical resources in disadvantaged areas such as the Cijin district, and the prevalence of MetS in Taiwan. We used two representative secondary cross-sectional datasets, including physical examinations and lifestyle surveys from 2016 to 2020, sourced from the Taiwan Biobank and the Cijin District Adult Lifestyle and Health Survey. Our findings indicate that residing in the Cijin district, characterized by socioeconomic deprivation and limited medical resources, is associated with significantly higher odds of MetS (aOR = 1.45, 95% CI = 1.28-1.64, p <0.001). Additionally, living in areas with medium (aOR = 1.12, 95% CI = 1.07-1.17, p <0.001) and high area-level socioeconomic deprivation indexes (aOR = 1.13, 95% CI = 1.01-1.25, p <0.001) is linked to a higher likelihood of MetS. Conversely, residing in high medical resource availability index areas is associated with a lower risk of MetS (aOR = 0.92, 95% CI = 0.86-0.99, p = 0.026). We found a link between socioeconomic deprivation and limited medical resources, especially in disadvantaged areas such as the Cijin district, contributing to a higher MetS risk. Residents in these areas often struggle to access healthcare and preventive care. Addressing these disparities requires comprehensive public health initiatives and targeted policy interventions to improve residents' well-being.</p>","PeriodicalId":94244,"journal":{"name":"The Kaohsiung journal of medical sciences","volume":" ","pages":"1106-1117"},"PeriodicalIF":0.0,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11618489/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142635632","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Diagnostic value of sFlt-1/PlGF-1 ratio and plasma PROK1 for adverse pregnancy outcomes in women with hypertensive disease of pregnancy.
The Kaohsiung journal of medical sciences Pub Date : 2024-12-01 Epub Date: 2024-12-03 DOI: 10.1002/kjm2.12907
Ping Lv, Lin-Fei Lu
{"title":"Diagnostic value of sFlt-1/PlGF-1 ratio and plasma PROK1 for adverse pregnancy outcomes in women with hypertensive disease of pregnancy.","authors":"Ping Lv, Lin-Fei Lu","doi":"10.1002/kjm2.12907","DOIUrl":"10.1002/kjm2.12907","url":null,"abstract":"<p><p>Hypertensive disease of pregnancy (HDP) is one of the most important causes of increased maternal mortality and perinatal complications during pregnancy. We investigated the pregnancy outcomes of 156 HDP patients (65 gestational hypertension [GH], 13 chronic hypertension [CH], 74 preeclampsia-eclampsia [PE-EC], and 4 superimposed on PE [CH with PE]). In patients with different types of HDP, levels of soluble fms like tyrosine kinase-1 (sFlt-1), placental growth factor (PlGF)-1, and prokinin-1 (PROK1) were measured and compared. The predictive efficacy of these indicators was evaluated using receiving operating characteristics curves and area under the curve. Results showed that the PE cohort had a higher sFlt-1/PlGF ratio (46.12 [39.24, 68.85]) and PROK1 (498.84 [213.67, 678.30] pg/mL) level than the GH (sFlt-1/PlGF, 32.3 [21.98, 58.00], PROK1 300.77[250.0, 345.29]pg/mL) and CH cohort (sFlt-1/PlGF, 37.49 [32.68, 39.68], PROK1, 281.48 [229.25, 453.94]pg/mL). In the HDP cohort, 54 patients experienced adverse pregnancy events, and the sFlt-1/PlGF ratio, PROK1, and the combined indicators (sFlt-1/PlGF ratio and PROK1) were excellent predictors of adverse pregnancy events, especially for PE patients.</p>","PeriodicalId":94244,"journal":{"name":"The Kaohsiung journal of medical sciences","volume":" ","pages":"1068-1076"},"PeriodicalIF":0.0,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11618490/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142776132","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
ELAVL1-dependent SOAT2 exacerbated the pancreatitis-like cellular injury of AR42J cells induced by hyperstimulation with caerulein. ELAVL1依赖的SOAT2加剧了AR42J细胞在caerulein过度刺激下诱发的胰腺炎样细胞损伤。
The Kaohsiung journal of medical sciences Pub Date : 2024-11-26 DOI: 10.1002/kjm2.12911
Yu-Jing Sun, Hua-Ying Chen, Xiao-Qin Lai
{"title":"ELAVL1-dependent SOAT2 exacerbated the pancreatitis-like cellular injury of AR42J cells induced by hyperstimulation with caerulein.","authors":"Yu-Jing Sun, Hua-Ying Chen, Xiao-Qin Lai","doi":"10.1002/kjm2.12911","DOIUrl":"https://doi.org/10.1002/kjm2.12911","url":null,"abstract":"<p><p>Pancreatitis is a severe inflammatory condition characterized by damage to the pancreas. Sterol o-acyltransferase 2 (SOAT2) has been reported to aggravate acute pancreatitis, however, the underlying mechanism remains to be elucidated. Rat pancreatic exocrine cells (AR42J) were treated with caerulein to induce pancreatitis-like cellular injury. Cell viability was determined using a cell counting kit-8 (CCK-8) assay, while cell proliferation was analyzed through a 5-Ethynyl-2'-deoxyuridine assay. Cell apoptosis was measured using flow cytometry, and enzyme-linked immunosorbent assays were performed to detect levels of pro-inflammatory cytokines IL-6 and TNF-α. Additionally, Fe<sup>2+</sup> levels were analyzed using a colorimetric assay kit, reactive oxygen species (ROS) levels were assessed with a Cellular ROS Assay kit, and lipid peroxidation was measured using a malondialdehyde assay kit. Glutathione levels were analyzed with a detection assay. Protein and mRNA expression were evaluated through western blotting and quantitative real-time polymerase chain reaction, respectively. Furthermore, an RNA immunoprecipitation assay was conducted to investigate the association between ELAV-like RNA binding protein 1 (ELAVL1) and SOAT2. Actinomycin D assay was performed to explore the effect of ELAVL1 depletion on the transcript stability of SOAT2 mRNA. SOAT2 and ELAVL1 expression were upregulated in caerulein-exposed AR42J cells. Caerulein treatment induced pancreatitis-like cellular apoptosis, inflammatory response, ferroptosis, and cell proliferation inhibition. Silencing of SOAT2 protected against caerulein-induced AR42J cell injury. Moreover, ELAVL1 stabilized SOAT2 mRNA expression in AR42J cells. SOAT2 overexpression attenuated the effects induced by ELAVL1 silencing in caerulein-exposed AR42J cells. Additionally, ELAVL1 knockdown activated the NRF2/HO-1 pathway by downregulating SOAT2 expression in caerulein-exposed AR42J cells. SOAT2 silencing protected AR42J cells from caerulein-induced injury by inactivating the NRF2 pathway. In conclusion, ELAVL1-dependent SOAT2 exacerbated pancreatic exocrine cell injury by inactivating the NRF2/HO-1 pathway in pancreatitis. These findings provide new insights into the molecular mechanisms underlying pancreatitis and offer potential therapeutic targets for the treatment of this condition.</p>","PeriodicalId":94244,"journal":{"name":"The Kaohsiung journal of medical sciences","volume":" ","pages":"e12911"},"PeriodicalIF":0.0,"publicationDate":"2024-11-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142718035","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Mitochondrial DNA copy number as a mediator of the relationship between insulin resistance and cognitive function in patients with euthymic bipolar disorder. 线粒体 DNA 拷贝数是嗜睡型双相情感障碍患者胰岛素抵抗与认知功能之间关系的介导因素。
The Kaohsiung journal of medical sciences Pub Date : 2024-11-23 DOI: 10.1002/kjm2.12914
Tsung-Han Tsai, Cheng Ying Wu, Cheng-Chen Chang, Ta-Tsung Lin, Chin-San Liu, Po See Chen
{"title":"Mitochondrial DNA copy number as a mediator of the relationship between insulin resistance and cognitive function in patients with euthymic bipolar disorder.","authors":"Tsung-Han Tsai, Cheng Ying Wu, Cheng-Chen Chang, Ta-Tsung Lin, Chin-San Liu, Po See Chen","doi":"10.1002/kjm2.12914","DOIUrl":"https://doi.org/10.1002/kjm2.12914","url":null,"abstract":"<p><p>Persistent cognitive challenges in bipolar disorder (BD) may be tied to insulin resistance, which crucially affects both metabolism and brain health. Additionally, mitochondrial DNA (mtDNA) copy number has emerged as an indicator of cognitive performance and response to treatment in BD. However, it remains unclear whether and how this indicator might serve as a bridge between metabolic dysfunction and cognitive capacity. In 68 study participants with euthymic BD, insulin resistance was assessed according to fasting glucose and insulin levels. mtDNA copy number was quantified from leukocytes, and executive function was measured with the Wisconsin card-sorting test (WCST). Mediation models were applied to explore the statistical relationship between insulin resistance, mtDNA copy number, and executive function. Both linear regression and Poisson distribution approaches with robust bootstrap simulations were used for significance testing. The results indicated that insulin resistance indirectly affects executive function via mtDNA copy number. This mediation relationship was statistically significant for both preservation errors and completion of categories in the WCST, although there were no significant direct effects of insulin resistance on the executive functions. We therefore concluded that insulin resistance is associated with reduced mtDNA copy number in blood, which may negatively impact executive functions in patients with euthymic BD. Further work is warranted to determine if improving metabolic and mitochondrial health may lead to better cognitive outcomes in BD.</p>","PeriodicalId":94244,"journal":{"name":"The Kaohsiung journal of medical sciences","volume":" ","pages":"e12914"},"PeriodicalIF":0.0,"publicationDate":"2024-11-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142696296","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Higher skin sympathetic nerve activity as a potential predictor of overactive bladder in females refractory to oral monotherapy. 较高的皮肤交感神经活性是口服单一疗法难治性女性膀胱过度活动症的潜在预测因素。
The Kaohsiung journal of medical sciences Pub Date : 2024-11-01 Epub Date: 2024-10-09 DOI: 10.1002/kjm2.12899
Yu-Chen Chen, Hao-Wei Chen, Tien-Chi Huang, Chien-Hung Lee, Ting-Yin Chu, Yung-Shun Juan, Yu-Peng Liu, Wei-Chung Tsai, Wen-Jeng Wu
{"title":"Higher skin sympathetic nerve activity as a potential predictor of overactive bladder in females refractory to oral monotherapy.","authors":"Yu-Chen Chen, Hao-Wei Chen, Tien-Chi Huang, Chien-Hung Lee, Ting-Yin Chu, Yung-Shun Juan, Yu-Peng Liu, Wei-Chung Tsai, Wen-Jeng Wu","doi":"10.1002/kjm2.12899","DOIUrl":"10.1002/kjm2.12899","url":null,"abstract":"<p><p>This study investigates predictors of unsatisfactory outcomes in female overactive bladder (OAB) patients treated with oral monotherapy by analyzing skin sympathetic nerve activity (SKNA) using a novel \"neuECG\" method. The study included 55 newly diagnosed female patients with idiopathic OAB, autonomic function was evaluated using neuECG before treatment initiation, and validated OAB questionnaires and urodynamic studies were administered. Initial monotherapy was administered for the first 4 weeks, with non-responders defined as patients not achieving satisfactory symptom relief and requiring further treatment. Responders (n = 32) and non-responders (n = 23) had no significant differences in baseline characteristics or urodynamic parameters; however, non-responders exhibited significantly higher baseline average SKNA (aSKNA) (1.36 ± 0.49 vs. 0.97 ± 0.29 μV, p = 0.001), higher recovery aSKNA (1.28 ± 0.46 vs. 0.97 ± 0.35 μV, p = 0.007), and a lower stress/baseline ratio of aSKNA (1.05 ± 0.42 vs. 1.26 ± 0.26, p = 0.029). Baseline aSKNA had the highest predictive value for monotherapy refractoriness in OAB (AUROC = 0.759, p = 0.001), with an optimal cut-off point of >1.032 μV. These findings suggest that elevated pre-treatment aSKNA can predict resistance to oral monotherapy in OAB, warranting close monitoring and proactive treatment strategies for patients with high aSKNA.</p>","PeriodicalId":94244,"journal":{"name":"The Kaohsiung journal of medical sciences","volume":" ","pages":"1020-1028"},"PeriodicalIF":0.0,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142396489","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Long non-coding RNA MALAT1 triggers ferroptosis via interaction with FUS to enhance ACSF2 mRNA stabilization in septic acute kidney injury. 长非编码 RNA MALAT1 在脓毒症急性肾损伤中通过与 FUS 相互作用引发铁凋亡,从而增强 ACSF2 mRNA 的稳定性。
The Kaohsiung journal of medical sciences Pub Date : 2024-11-01 Epub Date: 2024-10-10 DOI: 10.1002/kjm2.12898
Zhi-Bing Duan, Ji-Fu Zheng, Si-Yue Huang, Li-Li Hu
{"title":"Long non-coding RNA MALAT1 triggers ferroptosis via interaction with FUS to enhance ACSF2 mRNA stabilization in septic acute kidney injury.","authors":"Zhi-Bing Duan, Ji-Fu Zheng, Si-Yue Huang, Li-Li Hu","doi":"10.1002/kjm2.12898","DOIUrl":"10.1002/kjm2.12898","url":null,"abstract":"<p><p>Septic acute kidney injury (AKI) is a fatal disease in the intensive care unit, with ferroptosis playing a crucial role in its pathogenesis. Long non-coding RNA (LncRNA) metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) has been implicated in septic-induced AKI inflammation and apoptosis. However, its regulatory role in ferroptosis and underlying mechanisms remain unclear. In vivo and in vitro models of septic AKI were established using cecal ligation and puncture (CLP) and lipopolysaccharide (LPS) challenge, respectively. Serum levels of creatinine (Cr), blood urea nitrogen (BUN), kidney injury molecule-1 (Kim-1), neutrophil gelatinase-associated lipocalin (NGAL), and inflammatory cytokine in kidney tissues were determined by ELISA kits. Histopathological alterations and apoptosis were evaluated by HE staining and TUNEL. Ferroptosis was accessed by measuring MDA, GSH, Fe<sup>2+</sup>, total and lipid ROS levels, and mitochondrial ultrastructure changes. Target molecular levels were determined using RT-qPCR, Western blotting, and immunofluorescence. Interactions among MALAT1, acyl-CoA synthetase family member 2 (ACSF2) and FUS RNA binding protein (FUS) were validated by RIP and RNA-pull down. MALAT1 level was significantly elevated in both in vivo and in vitro septic AKI models, of which knockdown impeded ferroptosis to alleviate septic AKI. Mechanistically, high MALAT1 expression increased ACSF2 mRNA stability via interaction with FUS. Rescue experiments showed that ACSF2 overexpression partially reversed the ferroptosis inhibition mediated by MALAT1 silencing. MALAT1 induces ferroptosis and exacerbates septic AKI by stabilizing ACSF2 mRNA with the assistance of FUS. These findings provide theoretical evidence for MALAT1 as a potential therapeutic target for septic AKI.</p>","PeriodicalId":94244,"journal":{"name":"The Kaohsiung journal of medical sciences","volume":" ","pages":"972-984"},"PeriodicalIF":0.0,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142402608","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Complement factor B inhibitor LNP023 mediates the effect and mechanism of AMPK/mTOR on autophagy and oxidative stress in lupus nephritis. 补体因子B抑制剂LNP023介导AMPK/mTOR对狼疮肾炎自噬和氧化应激的影响及其机制
The Kaohsiung journal of medical sciences Pub Date : 2024-11-01 Epub Date: 2024-10-12 DOI: 10.1002/kjm2.12894
Xi-Mei Zhang, Ming-Jie Qing, Xin-Kuo Liu, Liang Peng
{"title":"Complement factor B inhibitor LNP023 mediates the effect and mechanism of AMPK/mTOR on autophagy and oxidative stress in lupus nephritis.","authors":"Xi-Mei Zhang, Ming-Jie Qing, Xin-Kuo Liu, Liang Peng","doi":"10.1002/kjm2.12894","DOIUrl":"10.1002/kjm2.12894","url":null,"abstract":"<p><p>This study investigated the impact of LNP023 on the AMPK/mTOR signaling pathway in lupus nephritis (LN) and its effects on autophagy and oxidative stress. A mouse model of LN was established, and renal injury was confirmed by assessing various LN markers, including antinuclear antibody, ds-DNA, anti-Sm antibody, and others. Mice were treated with LNP023, the AMPK activator AICAR, or the AMPK inhibitor dorsomorphin. Renal injury and fibrosis were evaluated using HE and Masson staining. Expression levels of AMPK, mTOR, LC3, Beclin1, and p62 were assessed by immunohistochemistry and Western blot. Oxidative stress and inflammatory markers were measured by polymerase chain reaction and enzyme-linked immunosorbent assay. LN mice exhibited low AMPK/p-AMPK and high mTOR/p-mTOR levels, alongside significant renal injury, fibrosis, reduced autophagy, and elevated oxidative stress. LNP023 treatment improved these parameters, with enhanced effects when combined with AICAR. Conversely, dorsomorphin reversed LNP023's therapeutic benefits. The complement factor B inhibitor LNP023 promotes kidney health in LN mice by mediating the AMPK/mTOR pathway, promoting autophagy, and attenuating oxidative stress.</p>","PeriodicalId":94244,"journal":{"name":"The Kaohsiung journal of medical sciences","volume":" ","pages":"996-1005"},"PeriodicalIF":0.0,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142484783","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Berberine safeguards sepsis-triggered acute gastric damage and inhibits pyroptosis in gastric epithelial cells via suppressing the ubiquitination and degradation of Nrf2. 小檗碱能保护败血症引发的急性胃损伤,并通过抑制 Nrf2 的泛素化和降解抑制胃上皮细胞的脓毒症。
The Kaohsiung journal of medical sciences Pub Date : 2024-11-01 DOI: 10.1002/kjm2.12900
Shu-Rui Xie, Yan-Jun Liu, Fen-Qiao Chen, Zhao Pan
{"title":"Berberine safeguards sepsis-triggered acute gastric damage and inhibits pyroptosis in gastric epithelial cells via suppressing the ubiquitination and degradation of Nrf2.","authors":"Shu-Rui Xie, Yan-Jun Liu, Fen-Qiao Chen, Zhao Pan","doi":"10.1002/kjm2.12900","DOIUrl":"10.1002/kjm2.12900","url":null,"abstract":"<p><p>Berberine (BBR), a widely recognized traditional Chinese medicine, has attracted considerable attention for its promising anti-inflammatory effects. The activation of nuclear factor erythroid 2-related factor 2 (Nrf2) effectively safeguards against organ damage stemming from sepsis-induced oxidative stress and inflammatory responses. This study examined the potential of BBR in alleviating sepsis-induced acute gastric injury, with a particular focus on elucidating whether its mechanism of action involves the activation of the Nrf2 signaling pathway. Following intraperitoneal injection of BBR, mice were subjected to the cecal ligation and puncture (CLP) method to induce sepsis. In vitro experiments involved pre-treating the normal gastric epithelial cells (GES-1) with BBR, followed by treatment with lipopolysaccharide (LPS). Functional assays were then performed to assess cell proliferation and apoptosis. To validate the role of Nrf2 in pyroptosis and inflammation, siRNA targeting Nrf2 (si-Nrf2) was transfected into LPS-treated GES-1 cells. Additionally, mice were administered the Nrf2 inhibitor ML385 to confirm the protective effects of BBR in vivo. BBR displayed a dose-dependent effect in mitigating gastric tissue damage, suppressing the release of inflammatory cytokines, and reducing the expression of NLRP3, ASC, and GSDMD-N. In vitro, BBR fostered GES-1 cell proliferation, hindered apoptosis, and suppressed the levels of TNF-α, IL-18, IL-1β, NLRP3, ASC, and GSDMD-N. Further analysis revealed that knocking down Nrf2 reversed BBR's inhibitory effect on pyroptosis in LPS-treated GES-1 cells. Through binding to Keap1, BBR efficiently prevented the ubiquitination and degradation of Nrf2, ultimately promoting its nuclear translocation. In vivo experiments confirmed that ML385 reversed the protective effect of BBR on pyroptosis and inflammation. Our research reveals that BBR interacts with Keap1 to activate the Keap1/Nrf2 signaling pathway in gastric epithelial cells, thereby suppressing pyroptosis and inflammation in sepsis-induced acute gastric injury.</p>","PeriodicalId":94244,"journal":{"name":"The Kaohsiung journal of medical sciences","volume":" ","pages":"1006-1019"},"PeriodicalIF":0.0,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142559927","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
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