Journal of Biomedical Research最新文献

{"title":"Extradural contralateral S1 nerve root transfer for spastic lower limb paralysis.","authors":"Jiang Cao,&nbsp;Jie Chang,&nbsp;Chaoqin Wu,&nbsp;Sheng Zhang,&nbsp;Binyu Wang,&nbsp;Kaixiang Yang,&nbsp;Xiaojian Cao,&nbsp;Tao Sui","doi":"10.7555/JBR.37.20230068","DOIUrl":"10.7555/JBR.37.20230068","url":null,"abstract":"<p><p>The current study aims to ascertain the anatomical feasibility of transferring the contralateral S1 ventral root (VR) to the ipsilateral L5 VR for treating unilateral spastic lower limb paralysis. Six formalin-fixed (three males and three females) cadavers were used. The VR of the contralateral S1 was transferred to the VR of the ipsilateral L5. The sural nerve was selected as a bridge between the donor and recipient nerve. The number of axons, the cross-sectional areas and the pertinent distances between the donor and recipient nerves were measured. The extradural S1 VR and L5 VR could be separated based on anatomical markers of the dorsal root ganglion. The gross distance between the S1 nerve root and L5 nerve root was 31.31 (± 3.23) mm in the six cadavers, while that on the diffusion tensor imaging was 47.51 (± 3.23) mm in 60 patients without spinal diseases, and both distances were seperately greater than that between the outlet of S1 from the spinal cord and the ganglion. The numbers of axons in the S1 VRs and L5 VRs were 13414.20 (± 2890.30) and 10613.20 (± 2135.58), respectively. The cross-sectional areas of the S1 VR and L5 VR were 1.68 (± 0.26) mm ² and 1.08 (± 0.26) mm ², respectively. In conclusion, transfer of the contralateral S1 VR to the ipsilateral L5 VR may be an anatomically feasible treatment option for unilateral spastic lower limb paralysis.</p>","PeriodicalId":15061,"journal":{"name":"Journal of Biomedical Research","volume":" ","pages":"394-400"},"PeriodicalIF":0.0,"publicationDate":"2023-09-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10541774/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41177563","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":"A novel synthesized prodrug of gemcitabine based on oxygen-free radical sensitivity inhibited the growth of lung cancer cells.","authors":"Xinlu Chai,&nbsp;Yuting Meng,&nbsp;Wei Ge,&nbsp;Juan Wang,&nbsp;Fei Li,&nbsp;Xue Jun Wang,&nbsp;Xuerong Wang","doi":"10.7555/JBR.37.20230022","DOIUrl":"10.7555/JBR.37.20230022","url":null,"abstract":"<p><p>In the present study, we introduced the H ₂O ₂-sensitive thiazolidinone moiety at the 4th amino group of gemcitabine (GEM) to synthesize a new target compound named GEM-ZZQ, and then we confirmed its chemical structure by nuclear magnetic resonance spectroscopy. We further confirmed that GEM-ZZQ had a good chemical stability in different pH solutions <i>in vitro</i> and that it could be activated by H ₂O ₂ to release GEM. Pharmacodynamic studies revealed that the growth inhibition of human normal epithelial cells was weaker by GEM-ZZQ than by GEM treatment and that the inhibition of various lung cancer cell lines by GEM-ZZQ was similar to that of GEM. For the lung cancer cell lines that are resistant to the epidermal growth factor receptor (EGFR)-targeting inhibitor osimertinib, GEM-ZZQ showed less growth inhibition than GEM; however, GEM-ZZQ in combination with cisplatin showed better synergistic effects than GEM in the low-dose groups. In summary, we provided a new anti-cancer compound GEM-ZZQ for treating lung cancer by modifying the GEM structure.</p>","PeriodicalId":15061,"journal":{"name":"Journal of Biomedical Research","volume":" ","pages":"355-366"},"PeriodicalIF":2.3,"publicationDate":"2023-09-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10541775/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10234957","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":"HSP90B1-mediated plasma membrane localization of GLUT1 promotes radioresistance of glioblastomas.","authors":"Yanhui Li,&nbsp;Yuqian Ge,&nbsp;Mengjie Zhao,&nbsp;Fangshu Ding,&nbsp;Xiuxing Wang,&nbsp;Zhumei Shi,&nbsp;Xin Ge,&nbsp;Xiefeng Wang,&nbsp;Xu Qian","doi":"10.7555/JBR.37.20220234","DOIUrl":"10.7555/JBR.37.20220234","url":null,"abstract":"<p><p>Ionizing radiation is a popular and effective treatment option for glioblastoma (GBM). However, resistance to radiation therapy inevitably occurs during treatment. It is urgent to investigate the mechanisms of radioresistance in GBM and to find ways to improve radiosensitivity. Here, we found that heat shock protein 90 beta family member 1 (HSP90B1) was significantly upregulated in radioresistant GBM cell lines. More importantly, HSP90B1 promoted the localization of glucose transporter type 1, a key rate-limiting factor of glycolysis, on the plasma membrane, which in turn enhanced glycolytic activity and subsequently tumor growth and radioresistance of GBM cells. These findings imply that targeting HSP90B1 may effectively improve the efficacy of radiotherapy for GBM patients, a potential new approach to the treatment of glioblastoma.</p>","PeriodicalId":15061,"journal":{"name":"Journal of Biomedical Research","volume":" ","pages":"326-339"},"PeriodicalIF":0.0,"publicationDate":"2023-09-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10541777/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41175606","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":"Association of maternal hypertensive disorders in pregnancy with infant neurodevelopment.","authors":"Bo Huang, Yifan Wang, Yangqian Jiang, Hong Lv, Tao Jiang, Yun Qiu, Qun Lu, Jiangbo Du, Yuan Lin, Hongxia Ma","doi":"10.7555/JBR.37.20230074","DOIUrl":"10.7555/JBR.37.20230074","url":null,"abstract":"<p><p>Inconsistent findings have been reported regarding the associations between hypertensive disorders in pregnancy (HDP) and infant neurodevelopment. Leveraging data from the Jiangsu Birth Cohort, in the present study, we re-visited such associations in one-year-old infants from 2576 singleton pregnancies and 261 twin pregnancies. We first assessed infant neurodevelopment by the Bayley Scales of Infant and Toddler Development Screening Test (the Third Edition), and then estimated its association with maternal HDP using general linear regression models and Poisson regression models. In singleton pregnancies, compared with mothers unexposed to HDP, infants born to mothers with chronic hypertension exhibited a lower score ( <i>β</i>, -0.67; 95% confidence interval [CI], -1.19--0.15) and a higher risk of \"non-optimal\" gross motor development (risk ratio [RR], 2.21; 95% CI, 1.02-4.79); in twin pregnancies, infants born to mothers with HDP exhibited lower scores in cognition ( <i>β</i>, -0.49; 95% CI, -0.96--0.01), receptive communication ( <i>β</i>, -0.55; 95% CI, -1.03--0.06), and gross motor ( <i>β</i>, -0.44; 95% CI, -0.86--0.03), and at a higher risk of \"non-optimal\" gross motor development (RR, 2.12; 95% CI, 1.16-3.88). These findings indicate that infants born to mothers with HDP may have inferior neurodevelopment outcomes at the age of one year.</p>","PeriodicalId":15061,"journal":{"name":"Journal of Biomedical Research","volume":" ","pages":"479-491"},"PeriodicalIF":0.0,"publicationDate":"2023-09-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10687531/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41158691","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":"Paravertebral block for analgesia following excision of osteochondroma of the scapula: A case report.","authors":"Deepthi L Penta, Usha Saldanha, Hong Liu","doi":"10.7555/JBR.37.20230048","DOIUrl":"10.7555/JBR.37.20230048","url":null,"abstract":"<p><p>Scapular surgery has mainly been studied in the setting of fractures; regional anesthesia can be utilized as part of a multimodal analgesia regimen for postoperative pain relief. Previous studies are limited to scapular fracture pain. The available literature supports the use of various types of nerve blocks and even combinations of different blocks, of which the paravertebral nerve block is one such block that has been effective. We present a case of a patient undergoing excision of a scapular osteochondroma who received a single-shot paravertebral nerve block after surgery with an effective analgesia.</p>","PeriodicalId":15061,"journal":{"name":"Journal of Biomedical Research","volume":" ","pages":"401-404"},"PeriodicalIF":2.3,"publicationDate":"2023-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10541773/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10234955","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":"Elevated extracellular calcium ions accelerate the proliferation and migration of HepG2 cells and decrease cisplatin sensitivity.","authors":"Haozhe Xu,&nbsp;Yiming Zhou,&nbsp;Jing Guo,&nbsp;Tao Ling,&nbsp;Yujie Xu,&nbsp;Ting Zhao,&nbsp;Chuanxin Shi,&nbsp;Zhongping Su,&nbsp;Qiang You","doi":"10.7555/JBR.37.20230067","DOIUrl":"10.7555/JBR.37.20230067","url":null,"abstract":"<p><p>Hepatoblastoma is the most frequent liver malignancy in children. HepG2 has been discovered as a hepatoblastoma-derived cell line and tends to form clumps in culture. Intriguingly, we observed that the addition of calcium ions reduced cell clumping and disassociated HepG2 cells. The calcium signal is in connection with a series of processes critical in the tumorigenesis. Here, we demonstrated that extracellular calcium ions induced morphological changes and enhanced the epithelial-mesenchymal transition in HepG2 cells. Mechanistically, calcium ions promoted HepG2 proliferation and migration by up-regulating the phosphorylation levels of focal adhesion kinase (FAK), protein kinase B, and p38 mitogen-activated protein kinase. The inhibitor of FAK or Ca ²⁺/calmodulin-dependent kinase Ⅱ (CaMKⅡ) reversed the Ca ²⁺-induced effects on HepG2 cells, including cell proliferation and migration, epithelial-mesenchymal transition protein expression levels, and phosphorylation levels of FAK and protein kinase B. Moreover, calcium ions decreased HepG2 cells' sensitivity to cisplatin. Furthermore, we found that the expression levels of <i>FAK</i> and <i>CaMKⅡ</i> were increased in hepatoblastoma. The group with high expression levels of <i>FAK</i> and <i>CaMKⅡ</i> exhibited significantly lower ImmunoScore as well as CD8 ⁺ T and NK cells. The expression of <i>CaMKⅡ</i> was positively correlated with that of <i>PDCD1</i> and <i>LAG3</i>. Correspondingly, the expression of <i>FAK</i> was negatively correlated with that of <i>TNFSF9</i>, <i>TNFRSF4</i>, and <i>TNFRSF18</i>. Collectively, extracellular calcium accelerates HepG2 cell proliferation and migration <i>via</i> FAK and CaMKⅡ and enhances cisplatin resistance. FAK and CaMKⅡ shape immune cell infiltration and responses in tumor microenvironments, thereby serving as potential targets for hepatoblastoma.</p>","PeriodicalId":15061,"journal":{"name":"Journal of Biomedical Research","volume":" ","pages":"340-354"},"PeriodicalIF":0.0,"publicationDate":"2023-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10541776/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41175605","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":"Do reactive oxygen species damage or protect the heart in ischemia and reperfusion? Analysis on experimental and clinical data.","authors":"Leonid N Maslov,&nbsp;Natalia V Naryzhnaya,&nbsp;Maria Sirotina,&nbsp;Alexandr V Mukhomedzyanov,&nbsp;Boris K Kurbatov,&nbsp;Alla A Boshchenko,&nbsp;Huijie Ma,&nbsp;Yi Zhang,&nbsp;Feng Fu,&nbsp;Jianming Pei,&nbsp;Viacheslav N Azev,&nbsp;Vladimir A Pereverzev","doi":"10.7555/JBR.36.20220261","DOIUrl":"https://doi.org/10.7555/JBR.36.20220261","url":null,"abstract":"<p><p>The role of reactive oxygen species (ROS) in ischemic and reperfusion (I/R) injury of the heart has been discussed for more than 40 years. It has been demonstrated that reperfusion triggers a multiple increase in free radical generation in the isolated heart. Antioxidants were found to have the ability to mitigate I/R injury of the heart. However, it is unclear whether their cardioprotective effect truly depends on the decrease of ROS levels in myocardial tissues. Since high doses and high concentrations of antioxidants were experimentally used, it is highly likely that the cardioprotective effect of antioxidants depends on their interaction not only with free radicals but also with other molecules. It has been demonstrated that the antioxidant N-2-mercaptopropionyl glycine or NDPH oxidase knockout abolished the cardioprotective effect of ischemic preconditioning. Consequently, there is evidence that ROS protect the heart against the I/R injury.</p>","PeriodicalId":15061,"journal":{"name":"Journal of Biomedical Research","volume":"37 4","pages":"268-280"},"PeriodicalIF":2.3,"publicationDate":"2023-07-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10387750/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9973117","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":"A historical literature review of coronary microvascular obstruction and intra-myocardial hemorrhage as functional/structural phenomena.","authors":"Leonid N Maslov,&nbsp;Natalia V Naryzhnaya,&nbsp;Sergey V Popov,&nbsp;Alexandr V Mukhomedzyanov,&nbsp;Ivan A Derkachev,&nbsp;Boris K Kurbatov,&nbsp;Andrey V Krylatov,&nbsp;Feng Fu,&nbsp;Jianming Pei,&nbsp;Vyacheslav V Ryabov,&nbsp;Evgenii V Vyshlov,&nbsp;Svetlana V Gusakova,&nbsp;Alla A Boshchenko,&nbsp;Akpay Sarybaev","doi":"10.7555/JBR.37.20230021","DOIUrl":"https://doi.org/10.7555/JBR.37.20230021","url":null,"abstract":"<p><p>The analysis of experimental data demonstrates that platelets and neutrophils are involved in the no-reflow phenomenon, also known as microvascular obstruction (MVO). However, studies performed in the isolated perfused hearts subjected to ischemia/reperfusion (I/R) do not suggest the involvement of microembolization and microthrombi in this phenomenon. The intracoronary administration of alteplase has been found to have no effect on the occurrence of MVO in patients with acute myocardial infarction. Consequently, the major events preceding the appearance of MVO in coronary arteries are independent of microthrombi, platelets, and neutrophils. Endothelial cells appear to be the target where ischemia can disrupt the endothelium-dependent vasodilation of coronary arteries. However, reperfusion triggers more pronounced damage, possibly mediated by pyroptosis. MVO and intra-myocardial hemorrhage contribute to the adverse post-infarction myocardial remodeling. Therefore, pharmacological agents used to treat MVO should prevent endothelial injury and induce relaxation of smooth muscles. Ischemic conditioning protocols have been shown to prevent MVO, with L-type Ca ²⁺ channel blockers appearing the most effective in treating MVO.</p>","PeriodicalId":15061,"journal":{"name":"Journal of Biomedical Research","volume":"37 4","pages":"281-302"},"PeriodicalIF":2.3,"publicationDate":"2023-07-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10387746/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10276125","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":"Editorial commentary on the special issue of cardiovascular diseases.","authors":"Editorial Board","doi":"10.7555/JBR.37.20230800","DOIUrl":"https://doi.org/10.7555/JBR.37.20230800","url":null,"abstract":"Cardiovascular disease (CVD) is the most common cause of death worldwide, which includes a group of disorders affecting the heart and blood vessels, leading to an increasingly heavy burden on the society. Although some mounting efforts have been made to explore epidemiology, pathology and pathogenesis, and risk assessment and prevention of CVD, our understanding, treatment and prevention of the complex CVD remain the tip of the iceberg and need further investigations. In this special issue, we have selected five different articles that are presenting recent advances in the study of CVD, particularly in myocardial function and coronary microvessels, involving sepsis-induced myocardial dysfunction, myocardial ischemia and reperfusion, and coronary microvascular obstruction. Zhu et al explored the mechanism of sepsis-induced myocardial dysfunction, and demonstrated that the knockdown of 11β-HSD1 alleviated endotoxemiainduced myocardial mitochondrial injury, oxidative stress, and inflammation through the AMPK/SIRT1/PGC1α pathway[1]. Zhou et al established an efficient myocardial ischemia/reperfusion (I/R) model in pigs through the median thoracic incision with a high success rate and homogeneity of the MI area, which provides a reference and a guiding significance for I/R preclinical research[2]. Naryzhnaya et al summarized antiarrhythmic, cardioprotective, and vasoprotective effects of chronic hypoxia on enhancing cardiac tolerance to I/R, which involves the complex cellular and molecular mechanisms, such as reactive oxygen species, hormones and humoral factors, kinases, KATP channels and mitochondria, providing a basis for the new therapeutic approaches in I/R[3]. Maslov and colleagues focused on the debate of the protective or negative role of ROS in I/R of the heart. They reviewed myocardial origin, production and roles of ROS, and antioxidants in clinical cardiological practice as well as pointed out that future studies using low concentrations of the selective freeradical scavengers with simultaneous detection of ROS production and cardiac injury in the isolated heart would be the key to solve the issue[4]. Besides, in another review article, they concentrated on the latest research progress of coronary microvascular obstruction and summarized the triggers, contributing factors and potential pathogenesis of microvascular obstruction from both experimental and clinical data, including endothelial cell injury, microembolization and microthrombi, platelet aggregation, reactive oxygen species and Ca2+ overload; they also discussed current clinical treatment of MVO to map the MVO from different perspectives for future investigations[5]. We hope the readers find this special issue interesting and intriguing.","PeriodicalId":15061,"journal":{"name":"Journal of Biomedical Research","volume":"37 4","pages":"229"},"PeriodicalIF":2.3,"publicationDate":"2023-07-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10387749/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10276119","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":"Knockdown of 11β-hydroxysteroid dehydrogenase type 1 alleviates LPS-induced myocardial dysfunction through the AMPK/SIRT1/PGC-1α pathway.","authors":"Dongmei Zhu,&nbsp;Lingli Luo,&nbsp;Hanjie Zeng,&nbsp;Zheng Zhang,&nbsp;Min Huang,&nbsp;Suming Zhou","doi":"10.7555/JBR.36.20220212","DOIUrl":"https://doi.org/10.7555/JBR.36.20220212","url":null,"abstract":"<p><p>Sepsis-induced myocardial dysfunction is primarily accompanied by severe sepsis, which is associated with high morbidity and mortality. 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1), encoded by <i>Hsd11b1</i>, is a reductase that can convert inactive cortisone into metabolically active cortisol, but the role of 11β-HSD1 in sepsis-induced myocardial dysfunction remains poorly understood. The current study aimed to investigate the effects of 11β-HSD1 on a lipopolysaccharide (LPS)-induced mouse model, in which LPS (10 mg/kg) was administered to wild-type C57BL/6J mice and 11β-HSD1 global knockout mice. We asscessed cardiac function by echocardiography, performed transmission electron microscopy and immunohistochemical staining to analyze myocardial mitochondrial injury and histological changes, and determined the levels of reactive oxygen species and biomarkers of oxidative stress. We also employed polymerase chain reaction analysis, Western blotting, and immunofluorescent staining to determine the expression of related genes and proteins. To investigate the role of 11β-HSD1 in sepsis-induced myocardial dysfunction, we used LPS to induce lentivirus-infected neonatal rat ventricular cardiomyocytes. We found that knockdown of 11β-HSD1 alleviated LPS-induced myocardial mitochondrial injury, oxidative stress, and inflammation, along with an improved myocardial function; furthermore, the depletion of 11β-HSD1 promoted the phosphorylation of adenosine 5'-monophosphate-activated protein kinase (AMPK), peroxisome proliferator-activated receptor gamma coactivator 1α (PGC-1α), and silent information regulator 1 (SIRT1) protein levels both <i>in vivo</i> and <i>in vitro</i>. Therefore, the suppression of 11β-HSD1 may be a viable strategy to improve cardiac function against endotoxemia challenges.</p>","PeriodicalId":15061,"journal":{"name":"Journal of Biomedical Research","volume":"37 4","pages":"303-314"},"PeriodicalIF":2.3,"publicationDate":"2023-05-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10387747/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10274602","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}