This study investigates the mechanism underlying the therapeutic effects of lycopene (Lyc) on lipopolysaccharide (LPS)-induced acute lung injury (ALI). ALI cell models were established using A549 cells treated with LPS. Cell viability was assessed using cell counting kit-8. ALI cells were treated with Lyc, mitochondrial autophagy inhibitor cyclosporine A (CsA), PTEN-induced kinase 1 (PINK1) activator Valinomycin, and reactive oxygen species (ROS) inhibitor N-acetylcysteine (NAC). Apoptosis was evaluated by flow cytometry and JC-1 probe staining. ROS and adenosine triphosphate levels were determined using dichloro-dihydro-fluorescein diacetate staining. Western blot assessed the expression levels of light chain 3 (LC3), Lysosomal-associated membrane protein 1, PINK1, and Parkin. An LPS-induced ALI rat model was treated with different concentrations of Lyc. Lung injury was assessed by hematoxylin and eosin staining. Levels of tumor necrosis factor-α, interleukin-6, and lactate dehydrogenase were measured by ELISA combined with magnetic nanoparticles. In this study, different concentrations of Lyc treatment enhanced cell survival. Additionally, Lyc treatment reduced the cell apoptosis rate, decreased lactate dehydrogenase (LDH) leakage and ROS level in ALI cells, and inhibited the expression of LC3, Beclin-1, PINK1, and Parkin. Consistent effects were seen in Lyc, CsA, Valinomycin, and NAC groups, suggesting similar impacts. In animal experiments, Lyc treatment significantly mitigated edema, inflammation, and autophagy in lung tissues. Furthermore, Lyc exhibited a protective effect on ALI cells by regulating PINK1/Parkin pathway and inhibiting mitochondrial autophagy. Overall, Lyc regulates mitochondrial autophagy in LPS-induced ALI with practical significance for studying its pharmacological mechanism and theoretical implications for understanding autophagy in ALI.
{"title":"Therapeutic Effects of Lycopene on Lipopolysaccharide-Induced Acute Lung Injury: Regulation of the PINK1/Parkin Signaling Pathway and Mitochondrial Autophagy","authors":"Benchao Hou, Lili Zhao, Jia Min, Xiuhong Wang, Jian Huang, Haimei Xia, Tianyin Liu","doi":"10.1166/jbn.2023.3729","DOIUrl":"https://doi.org/10.1166/jbn.2023.3729","url":null,"abstract":"This study investigates the mechanism underlying the therapeutic effects of lycopene (Lyc) on lipopolysaccharide (LPS)-induced acute lung injury (ALI). ALI cell models were established using A549 cells treated with LPS. Cell viability was assessed using cell counting kit-8. ALI cells\u0000 were treated with Lyc, mitochondrial autophagy inhibitor cyclosporine A (CsA), PTEN-induced kinase 1 (PINK1) activator Valinomycin, and reactive oxygen species (ROS) inhibitor N-acetylcysteine (NAC). Apoptosis was evaluated by flow cytometry and JC-1 probe staining. ROS and adenosine triphosphate\u0000 levels were determined using dichloro-dihydro-fluorescein diacetate staining. Western blot assessed the expression levels of light chain 3 (LC3), Lysosomal-associated membrane protein 1, PINK1, and Parkin. An LPS-induced ALI rat model was treated with different concentrations of Lyc. Lung\u0000 injury was assessed by hematoxylin and eosin staining. Levels of tumor necrosis factor-α, interleukin-6, and lactate dehydrogenase were measured by ELISA combined with magnetic nanoparticles. In this study, different concentrations of Lyc treatment enhanced cell survival. Additionally,\u0000 Lyc treatment reduced the cell apoptosis rate, decreased lactate dehydrogenase (LDH) leakage and ROS level in ALI cells, and inhibited the expression of LC3, Beclin-1, PINK1, and Parkin. Consistent effects were seen in Lyc, CsA, Valinomycin, and NAC groups, suggesting similar impacts. In animal\u0000 experiments, Lyc treatment significantly mitigated edema, inflammation, and autophagy in lung tissues. Furthermore, Lyc exhibited a protective effect on ALI cells by regulating PINK1/Parkin pathway and inhibiting mitochondrial autophagy. Overall, Lyc regulates mitochondrial autophagy in LPS-induced\u0000 ALI with practical significance for studying its pharmacological mechanism and theoretical implications for understanding autophagy in ALI.","PeriodicalId":15260,"journal":{"name":"Journal of biomedical nanotechnology","volume":" 7","pages":""},"PeriodicalIF":2.9,"publicationDate":"2023-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138617292","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}
Despite the efficacy of cryptotanshinone (CPT) against glioma, it has issues such as poor solubility and limited tumor penetration. To address these challenges, the development of a nano drug delivery system with high penetration and precise targeting is crucial. In this study, we utilized the emulsification-evaporation technique to create tLyp-1 modified liposomes that contain CPT. The tLyp-1 peptide, which is a membrane-penetrating agent, allows for precise targeting of brain glioma and drug release. We characterized the TLCP using particle size, polydispersity index (PDI), intracellular fluorescence, and transmission electron microscopy and found that it had a mean particle size of (169.1±22.0) nm and a PDI of 0.34±0.093. High performance liquid chromatography was used to quantify the encapsulation efficiency (74.33±8.9%). Our results showed that tLipo, the targeting liposome modified with tLyp-1, was taken up more by GL261 cells than regular liposomes. The intracellular fluorescence intensity of the tLipo group also increased. Fluorescence was observed in the mouse brain 0.5 h after tail vein injection of DiR-labeled tLipo, confirming its ability to penetrate the blood–brain barrier (BBB). The fluorescence was still present in the brain 24 h later. Our results further confirmed the BBB-penetration and anti-glioma efficacy of the nanodrug in reducing glioma cell growth.
{"title":"Enhancing Glioma Treatment by Using Novel Cryptotanshinone-Loaded Nano-Liposomes","authors":"Zuolin Shi, Mengjia Chen, Ligang Chen, Zheng Zou, Shun Gong, Guobiao Liang","doi":"10.1166/jbn.2023.3742","DOIUrl":"https://doi.org/10.1166/jbn.2023.3742","url":null,"abstract":"Despite the efficacy of cryptotanshinone (CPT) against glioma, it has issues such as poor solubility and limited tumor penetration. To address these challenges, the development of a nano drug delivery system with high penetration and precise targeting is crucial. In this study, we utilized\u0000 the emulsification-evaporation technique to create tLyp-1 modified liposomes that contain CPT. The tLyp-1 peptide, which is a membrane-penetrating agent, allows for precise targeting of brain glioma and drug release. We characterized the TLCP using particle size, polydispersity index (PDI),\u0000 intracellular fluorescence, and transmission electron microscopy and found that it had a mean particle size of (169.1±22.0) nm and a PDI of 0.34±0.093. High performance liquid chromatography was used to quantify the encapsulation efficiency (74.33±8.9%). Our results showed\u0000 that tLipo, the targeting liposome modified with tLyp-1, was taken up more by GL261 cells than regular liposomes. The intracellular fluorescence intensity of the tLipo group also increased. Fluorescence was observed in the mouse brain 0.5 h after tail vein injection of DiR-labeled tLipo, confirming\u0000 its ability to penetrate the blood–brain barrier (BBB). The fluorescence was still present in the brain 24 h later. Our results further confirmed the BBB-penetration and anti-glioma efficacy of the nanodrug in reducing glioma cell growth.","PeriodicalId":15260,"journal":{"name":"Journal of biomedical nanotechnology","volume":"38 1","pages":""},"PeriodicalIF":2.9,"publicationDate":"2023-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138621870","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}
Ying Liu, Qian Zhang, Li Wang, Yulong Wen, Xiaolan Jia
Myocardial ischemia-reperfusion (IR) in diabetes can cause severe myocardial damages. In this study, resveratrol (RES) nanoparticles were used in diabetic myocardial IR rat model injury to assess its effect on mitochondria function. Rat models were assigned into sham group, IR group, IR+RES group, IR+RES+mir-NC group, and IR+RES+miR-20b-5p inhibitor group. Myocardial infarction area was measured by TTC in 5 rats from each group, and ultrasound was used to detect left ventricular end-systolic internal diameters (LVIDs) and end-diastolic internal diameters (LVIDd), along with analysis of cardiomyopathy by HE staining. miR-20b-5p and Stromal interaction molecule 2 (STIM2) expressions, cardiomyocyte proliferation, apoptosis, cell viability, mitochondrial function, and relationship between miR-20b-5p and STIM2 were also analyzed. Resveratrol (RES) nanoparticles were prepared successfully. Myocardial infarct size, LVIDd and LVIDs of rats in IR+RES group decreased (vs. IR group), but were higher than sham group. miR-20b-5p expression also increased in the IR+RES group (vs. IR group), and the above indicators were decreased by the miR-20b-5p inhibitor (vs. IR+RES group, P <0.05). The myocardial changes in rats from the IR+RES+miR-20b-5p antagomir group were smaller (vs. IR group), while STIM2 expression was lower than in the IR group after using the RES nanoparticles (P < 0.05). RES nanoparticles can thus enhance mitochondrial function and cell viability of cardiomyocytes, increasing cell proliferation rate and decreasing apoptosis rate (vs. IR group,P <0.05). After using the RES nanoparticles to interfere with myocardial IR in the diabetic rats, they were found to inhibit STIM2 and improve mitochondria by regulating miR-20b-5p signaling pathway.
{"title":"Resveratrol Inhibited Nanoparticles Stromal Interaction Molecule 2 in Regulating miR-20b-5p Signaling Pathway to Improve Mitochondrial Function During Myocardial Ischemia-Reperfusion Injury","authors":"Ying Liu, Qian Zhang, Li Wang, Yulong Wen, Xiaolan Jia","doi":"10.1166/jbn.2023.3720","DOIUrl":"https://doi.org/10.1166/jbn.2023.3720","url":null,"abstract":"Myocardial ischemia-reperfusion (IR) in diabetes can cause severe myocardial damages. In this study, resveratrol (RES) nanoparticles were used in diabetic myocardial IR rat model injury to assess its effect on mitochondria function. Rat models were assigned into sham group, IR group,\u0000 IR+RES group, IR+RES+mir-NC group, and IR+RES+miR-20b-5p inhibitor group. Myocardial infarction area was measured by TTC in 5 rats from each group, and ultrasound was used to detect left ventricular end-systolic internal diameters (LVIDs) and end-diastolic internal diameters (LVIDd), along\u0000 with analysis of cardiomyopathy by HE staining. miR-20b-5p and Stromal interaction molecule 2 (STIM2) expressions, cardiomyocyte proliferation, apoptosis, cell viability, mitochondrial function, and relationship between miR-20b-5p and STIM2 were also analyzed. Resveratrol (RES) nanoparticles\u0000 were prepared successfully. Myocardial infarct size, LVIDd and LVIDs of rats in IR+RES group decreased (vs. IR group), but were higher than sham group. miR-20b-5p expression also increased in the IR+RES group (vs. IR group), and the above indicators were decreased by the miR-20b-5p inhibitor\u0000 (vs. IR+RES group, P <0.05). The myocardial changes in rats from the IR+RES+miR-20b-5p antagomir group were smaller (vs. IR group), while STIM2 expression was lower than in the IR group after using the RES nanoparticles (P < 0.05). RES nanoparticles can thus enhance mitochondrial\u0000 function and cell viability of cardiomyocytes, increasing cell proliferation rate and decreasing apoptosis rate (vs. IR group,P <0.05). After using the RES nanoparticles to interfere with myocardial IR in the diabetic rats, they were found to inhibit STIM2 and improve mitochondria\u0000 by regulating miR-20b-5p signaling pathway.","PeriodicalId":15260,"journal":{"name":"Journal of biomedical nanotechnology","volume":"119 15","pages":""},"PeriodicalIF":2.9,"publicationDate":"2023-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138609277","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}
In this study, by constructing a rat model of orthodontic recurrence and intervening with coptisine, the IL-6, IL-8, TNF-α and soluble intercellular adhesion molecule-1 (sICAM-1) content were analyzed to assess the regulatory mechanism of coptisine on the health status of recurrent periodontal tissue after orthodontics and the occurrence of periodontal tissue inflammation. Male rats were assigned into three groups by constructing coptisine liposome nano-objects: blank group (Blank, 10 rats), orthodontic tooth movement model group (50 rats). The orthodontic tooth movement model group was randomly divided into model group (module), model control group (control-free), model coptisine treatment group (treatment-free), model blank functional liposome group (control-lip) and model functional coptisine liposome group (treatment-lip). Rats in model group were killed on the day after device was removed. Rats in other groups received equal doses of normal saline, coptisine, blank functional liposomes, and functional coptisine liposomes by intragastric administration on the day of device removal and then were killed after 7 days of continuous treatment. Through Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis, we found that Fas/FasL signaling pathway was enriched in pathways related to apoptosis, disease infection and inflammation. Western blot experiments confirmed that coptisine could inhibit Fas/FasL signaling activation in the process of relapse after orthodontics. Lipopolysaccharides (LPS) treatment significantly increased inflammatory cytokines and sICAM-1, as well as the level of Fas and FasL. Coptisine treatment inhibited LPS-induced Fas/FasL signaling pathway in periodontal ligament cells. Coptisine attenuated the relapsed inflammation after orthodontics by inhibiting Fas/FasL signaling.
{"title":"Coptisine Down-Regulates Soluble Intercellular Adhesion Molecule-1 by Inactivating Fas/FasL Signaling Pathway to Inhibit the Recurrence After Orthodontics","authors":"Bing Song, Rui Gao, Xiaohui Xu, Weijun Yan","doi":"10.1166/jbn.2023.3718","DOIUrl":"https://doi.org/10.1166/jbn.2023.3718","url":null,"abstract":"In this study, by constructing a rat model of orthodontic recurrence and intervening with coptisine, the IL-6, IL-8, TNF-α and soluble intercellular adhesion molecule-1 (sICAM-1) content were analyzed to assess the regulatory mechanism of coptisine on the health status\u0000 of recurrent periodontal tissue after orthodontics and the occurrence of periodontal tissue inflammation. Male rats were assigned into three groups by constructing coptisine liposome nano-objects: blank group (Blank, 10 rats), orthodontic tooth movement model group (50 rats). The orthodontic\u0000 tooth movement model group was randomly divided into model group (module), model control group (control-free), model coptisine treatment group (treatment-free), model blank functional liposome group (control-lip) and model functional coptisine liposome group (treatment-lip). Rats in model\u0000 group were killed on the day after device was removed. Rats in other groups received equal doses of normal saline, coptisine, blank functional liposomes, and functional coptisine liposomes by intragastric administration on the day of device removal and then were killed after 7 days of continuous\u0000 treatment. Through Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis, we found that Fas/FasL signaling pathway was enriched in pathways related to apoptosis, disease infection and inflammation. Western blot experiments confirmed that coptisine could inhibit Fas/FasL signaling\u0000 activation in the process of relapse after orthodontics. Lipopolysaccharides (LPS) treatment significantly increased inflammatory cytokines and sICAM-1, as well as the level of Fas and FasL. Coptisine treatment inhibited LPS-induced Fas/FasL signaling pathway in periodontal ligament cells.\u0000 Coptisine attenuated the relapsed inflammation after orthodontics by inhibiting Fas/FasL signaling.","PeriodicalId":15260,"journal":{"name":"Journal of biomedical nanotechnology","volume":" 8","pages":""},"PeriodicalIF":2.9,"publicationDate":"2023-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138612414","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}
In the current study, mequinol was loaded into clay nanoparticles and the resulting nanocarriers were dispersed in a gelatin hydrogel to prepare a potential wound dressing material. The developed nanocomposite hydrogels were characterized regarding their biocompatibility, swelling, radical scavenging activity, swelling potential, and release profile. The healing function of the produce wound dressing was investigated in a rat model of diabetic wound healing. In vitro studies showed that our developed hydrogel was not toxic against the skin cells and was conductive for their adhesion and proliferation. In vivo study showed that mequinol-loaded nanocomposite hydrogels augmented the rate of wound size reduction in diabetic rats by improving wounds’ epithelialization and deposition of collagen fibers.
{"title":"Mequinol-Loaded Nano Clay Drug Carriers in a Gelatin Hydrogel for Wound Healing: An Antiinflammatory and Antioxidant Treatment Modality","authors":"Xiaoyan Sun, Yan Wang","doi":"10.1166/jbn.2023.3690","DOIUrl":"https://doi.org/10.1166/jbn.2023.3690","url":null,"abstract":"In the current study, mequinol was loaded into clay nanoparticles and the resulting nanocarriers were dispersed in a gelatin hydrogel to prepare a potential wound dressing material. The developed nanocomposite hydrogels were characterized regarding their biocompatibility, swelling,\u0000 radical scavenging activity, swelling potential, and release profile. The healing function of the produce wound dressing was investigated in a rat model of diabetic wound healing. In vitro studies showed that our developed hydrogel was not toxic against the skin cells and was conductive\u0000 for their adhesion and proliferation. In vivo study showed that mequinol-loaded nanocomposite hydrogels augmented the rate of wound size reduction in diabetic rats by improving wounds’ epithelialization and deposition of collagen fibers.","PeriodicalId":15260,"journal":{"name":"Journal of biomedical nanotechnology","volume":"123 26","pages":""},"PeriodicalIF":2.9,"publicationDate":"2023-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138609063","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}
Ovarian cancer (OC) incidence has in recent years been on the rise among common gynecological cancers. Iron oxide nanoparticles (IONPs), as emerging nanomedicines, have been widely used in research on cancer therapy. However, with in-depth research on microRNA (miRNA), the effect of combining miRNA with nanoparticles on ovarian cancer is not yet clear. We deeply explored the mechanism of IONPs loading miRNA to regulate ovarian cancer cells. In this study, novelmiR-21 inhibitor-IONPs nanoparticles were prepared by loading miR-21 inhibitor into IONPs. Electron microscopy was used to observe nano-encapsulation and miR-21 expression was measured along with analysis of cell proliferation, apoptosis by flow cytometry, and phosphorylation of apoptotic proteins and mitogen-activated protein kinase (MAPK) signaling pathways by Western blot. Our results showed that miR-21 inhibitor-IONPs reduced miR-21 expression, thereby inhibiting ovarian cancer cells activities and promoting apoptosis. miR-21 inhibitor-IONPs also inhibited p-p38MAPK and p-ERK levels, which were increased after addition of MAPK agonist (U-46619). Moreover, ovarian cancer cell proliferation increased and apoptosis decreased. miR-21 inhibitor-IONPs can thus inhibit MAPK signaling, thereby reducing the activities of ovarian cancer cells. This study provides theoretical support for application of miR-21 inhibitor-IONPs as novel nanoparticles for the treatment of ovarian cancer.
{"title":"Effect of miR-21 Inhibitor Coated with Ferric Oxide on Ovarian Cancer Cells Through Mitogen-Activated Protein Kinase Signaling Pathway","authors":"Weiwei Qian, Wen Feng","doi":"10.1166/jbn.2023.3726","DOIUrl":"https://doi.org/10.1166/jbn.2023.3726","url":null,"abstract":"Ovarian cancer (OC) incidence has in recent years been on the rise among common gynecological cancers. Iron oxide nanoparticles (IONPs), as emerging nanomedicines, have been widely used in research on cancer therapy. However, with in-depth research on microRNA (miRNA), the effect of\u0000 combining miRNA with nanoparticles on ovarian cancer is not yet clear. We deeply explored the mechanism of IONPs loading miRNA to regulate ovarian cancer cells. In this study, novelmiR-21 inhibitor-IONPs nanoparticles were prepared by loading miR-21 inhibitor into IONPs. Electron microscopy\u0000 was used to observe nano-encapsulation and miR-21 expression was measured along with analysis of cell proliferation, apoptosis by flow cytometry, and phosphorylation of apoptotic proteins and mitogen-activated protein kinase (MAPK) signaling pathways by Western blot. Our results showed that\u0000 miR-21 inhibitor-IONPs reduced miR-21 expression, thereby inhibiting ovarian cancer cells activities and promoting apoptosis. miR-21 inhibitor-IONPs also inhibited p-p38MAPK and p-ERK levels, which were increased after addition of MAPK agonist (U-46619). Moreover, ovarian cancer cell proliferation\u0000 increased and apoptosis decreased. miR-21 inhibitor-IONPs can thus inhibit MAPK signaling, thereby reducing the activities of ovarian cancer cells. This study provides theoretical support for application of miR-21 inhibitor-IONPs as novel nanoparticles for the treatment of ovarian cancer.","PeriodicalId":15260,"journal":{"name":"Journal of biomedical nanotechnology","volume":" 77","pages":""},"PeriodicalIF":2.9,"publicationDate":"2023-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138612054","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}
Contrast-induced acute kidney damage (CI-AKI) is a common side effect of diagnostic imaging treatments that use iodinated contrast medium, such as Iohexol. This potential threat to renal function may cause irreversible damage, particularly through pathways such as ferroptosis. Ferroptosis is a regulated form of cell death that relies heavily on iron and reactive oxygen species. Using in vitro experiments with HK-2 cells, our study investigated the cytotoxic effects of Iohexol, with a particular focus on its potential involvement in the ferroptosis pathway. To counteract this, we synthesized poly(lactic-coglycolic acid) (PLGA) nanoparticles loaded with butyric acid and ferrostatin against ferroptosis-mediated cell damage. We assessed lipid peroxidation using malondialdehyde (MDA) assays, and measured superoxide dismutase (SOD) activity to evaluate oxidative stress. We employed electron microscopy to examine ultrastructural changes. We also investigated the involvement of the Nuclear Factor Erythroid 2-Related Factor 2 (Nrf2)/Heme Oxygenase-1 (HO-1) pathway, which plays a crucial role in preserving cellular oxidative balance. At concentrations above 100 mg/mL, Iohexol significantly reduced the viability of HK-2 cells. However, this impact was alleviated by butyric acid and ferrostatin PLGA nanoparticles, highlighting the critical role of ferroptosis. Iohexol caused a significant increase in MDA levels, indicating heightened lipid peroxidation. However, the ferrostatin effectively suppressed this effect. Ultrastructural analysis revealed characteristic morphological changes associated with ferroptosis, including mitochondrial swelling and cristae disappearance. Moreover, we uncovered a novel association between the G protein-coupled receptor 41 and the ferroptosis pathway. Furthermore, we observed a significant interplay with the Nrf2/HO-1 signaling pathway. In conclusion, our study provides insights into the complex molecular mechanisms involved in Iohexol-induced nephrotoxicity, with a specific emphasis on ferroptosis and Nrf2/HO-1 signaling. These findings serve as a basis for the development of potential therapeutic strategies targeting ferroptosis in the context of CI-AKI.
{"title":"Potential Mechanisms of the Ferroptosis Pathway in Iohexol-Induced Renal Injury","authors":"Guokai Yang, Weitao Pan, Yanping Zu, Xian Yang","doi":"10.1166/jbn.2023.3719","DOIUrl":"https://doi.org/10.1166/jbn.2023.3719","url":null,"abstract":"Contrast-induced acute kidney damage (CI-AKI) is a common side effect of diagnostic imaging treatments that use iodinated contrast medium, such as Iohexol. This potential threat to renal function may cause irreversible damage, particularly through pathways such as ferroptosis. Ferroptosis\u0000 is a regulated form of cell death that relies heavily on iron and reactive oxygen species. Using in vitro experiments with HK-2 cells, our study investigated the cytotoxic effects of Iohexol, with a particular focus on its potential involvement in the ferroptosis pathway. To counteract\u0000 this, we synthesized poly(lactic-coglycolic acid) (PLGA) nanoparticles loaded with butyric acid and ferrostatin against ferroptosis-mediated cell damage. We assessed lipid peroxidation using malondialdehyde (MDA) assays, and measured superoxide dismutase (SOD) activity to evaluate oxidative\u0000 stress. We employed electron microscopy to examine ultrastructural changes. We also investigated the involvement of the Nuclear Factor Erythroid 2-Related Factor 2 (Nrf2)/Heme Oxygenase-1 (HO-1) pathway, which plays a crucial role in preserving cellular oxidative balance. At concentrations\u0000 above 100 mg/mL, Iohexol significantly reduced the viability of HK-2 cells. However, this impact was alleviated by butyric acid and ferrostatin PLGA nanoparticles, highlighting the critical role of ferroptosis. Iohexol caused a significant increase in MDA levels, indicating heightened lipid\u0000 peroxidation. However, the ferrostatin effectively suppressed this effect. Ultrastructural analysis revealed characteristic morphological changes associated with ferroptosis, including mitochondrial swelling and cristae disappearance. Moreover, we uncovered a novel association between the\u0000 G protein-coupled receptor 41 and the ferroptosis pathway. Furthermore, we observed a significant interplay with the Nrf2/HO-1 signaling pathway. In conclusion, our study provides insights into the complex molecular mechanisms involved in Iohexol-induced nephrotoxicity, with a specific emphasis\u0000 on ferroptosis and Nrf2/HO-1 signaling. These findings serve as a basis for the development of potential therapeutic strategies targeting ferroptosis in the context of CI-AKI.","PeriodicalId":15260,"journal":{"name":"Journal of biomedical nanotechnology","volume":" 14","pages":""},"PeriodicalIF":2.9,"publicationDate":"2023-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138612921","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}
Eccentric exercise (EE) may lead to skeletal muscle injury, including oxidative stress and inflammation induction. Ginsenoside Rg1, a glycosylated triterpene present in the traditional Chinese medicine ginseng, was previously shown to prevent the development of multiple diseases through the attenuation of oxidative stress and inflammation. Therefore, this article hopes to investigate whether Rg1 exhibits anti-oxidant and anti-inflammatory effects in eccentric exercise-induced muscle damage (EEIMD). Additionally, Adult male Wistar rats were intraperitoneally injected with Rg1 (20 or 40 mg/kg) every day before EE for 5 consecutive days. The impact of Rg1 administration on levels of serum creatine kinase was evaluated, followed by observation of histological muscle damage through H&E staining. To assess protein nitrotyrosylation, lipid peroxidation and leukocyte infiltration in rat skeletal muscles, the levels of nitrotyrosine, MDA and MPO protein were analysed through western blotting analysis. The inflammatory response was evaluated by detecting iNOS, COX-2, IL-1β, IL-6, MCP-1 and TNF-α mRNA and protein levels in rat skeletal muscles. The regulation of Rg1 on the NF-κB pathway was examined through the analysis of phosphorylated NF-κB p65 and IκBα protein levels. Result display, EE resulted in elevated serum creatine kinase levels, widespread leukocyte infiltration, and notable muscle cell vacuolization and fragmentation in muscles. Furthermore, EE increased nitrotyrosine, MDA, MPO, iNOS, COX-2, IL-1β, IL-6, MCP-1, and TNF-α levels in rats. However, these changes were reversed by Rg1 treatment. Furthermore, EE-induced upregulation in phosphorylated NF-κB p65 and IκBα levels was counteracted by Rg1. Overall, ginsenoside Rg1 plays an anti-oxidant and anti-inflammatory role in EEIMD through suppressing this NF-κB signaling pathway.
{"title":"Ginsenoside Rg1 Attenuates Eccentric Exercise-Induced Muscle Damage via the Modulation of Lipid Peroxidation and Inflammation","authors":"Qiong Zhang","doi":"10.1166/jbn.2023.3727","DOIUrl":"https://doi.org/10.1166/jbn.2023.3727","url":null,"abstract":"Eccentric exercise (EE) may lead to skeletal muscle injury, including oxidative stress and inflammation induction. Ginsenoside Rg1, a glycosylated triterpene present in the traditional Chinese medicine ginseng, was previously shown to prevent the development of multiple diseases through\u0000 the attenuation of oxidative stress and inflammation. Therefore, this article hopes to investigate whether Rg1 exhibits anti-oxidant and anti-inflammatory effects in eccentric exercise-induced muscle damage (EEIMD). Additionally, Adult male Wistar rats were intraperitoneally injected with\u0000 Rg1 (20 or 40 mg/kg) every day before EE for 5 consecutive days. The impact of Rg1 administration on levels of serum creatine kinase was evaluated, followed by observation of histological muscle damage through H&E staining. To assess protein nitrotyrosylation, lipid peroxidation and leukocyte\u0000 infiltration in rat skeletal muscles, the levels of nitrotyrosine, MDA and MPO protein were analysed through western blotting analysis. The inflammatory response was evaluated by detecting iNOS, COX-2, IL-1β, IL-6, MCP-1 and TNF-α mRNA and protein levels in rat skeletal\u0000 muscles. The regulation of Rg1 on the NF-κB pathway was examined through the analysis of phosphorylated NF-κB p65 and IκBα protein levels. Result display, EE resulted in elevated serum creatine kinase levels, widespread leukocyte infiltration,\u0000 and notable muscle cell vacuolization and fragmentation in muscles. Furthermore, EE increased nitrotyrosine, MDA, MPO, iNOS, COX-2, IL-1β, IL-6, MCP-1, and TNF-α levels in rats. However, these changes were reversed by Rg1 treatment. Furthermore, EE-induced upregulation\u0000 in phosphorylated NF-κB p65 and IκBα levels was counteracted by Rg1. Overall, ginsenoside Rg1 plays an anti-oxidant and anti-inflammatory role in EEIMD through suppressing this NF-κB signaling pathway.","PeriodicalId":15260,"journal":{"name":"Journal of biomedical nanotechnology","volume":" 1","pages":""},"PeriodicalIF":2.9,"publicationDate":"2023-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138615403","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}
We investigated the role of circ_0132269 in hepatocellular carcinoma (HCC). We examined circ_0132269 levels in HCC tissues and cell lines using qRT-PCR. Survival analysis was performed to assess the correlation between circ_0132269 expression and HCC patient survival rates. Knockdown of circ_0132269 was performed to evaluate its impact on HCC cell proliferation, migration, and invasion. Bioinformatics analysis predicted that circ_0132269 could interact with miR-1248. This interaction was confirmed using dual luciferase assays, and the correlation between circ_0132269 and miR-1248 was analyzed. Further functional experiments investigated the effect of miR-1248 on circ_0132269-mediated malignant phenotypes. circ_0132269 was significantly upregulated in HCC tissues and cell lines. Higher circ_0132269 expression correlated with poorer overall and disease-free survival in HCC patients. Silencing circ_0132269 suppressed HCC cell proliferation, migration, and invasion. Bioinformatics analysis revealed a binding site between circ_0132269 and miR-1248. miR-1248 expression was reduced in HCC, while its target MTO1 was highly expressed. miR-1248 levels showed a negative correlation with circ_0132269 and MTO1 levels, while circ_0132269 and MTO1 exhibited a positive correlation. Overexpression of miR-1248 partially reversed the promotive effect of highly expressed circ_0132269 on HCC cell behaviors. circ_0132269 was significantly upregulated in HCC and associated with poor prognosis. It interacts with miR-1248 to regulate HCC malignancy, highlighting its potential as a diagnostic and therapeutic target.
{"title":"Effects of Circ_0132269 on the Progression of Hepatocellular Carcinoma via Targeting miR-1248/MTO1","authors":"Peng Yu, Xiongwei Hu, Sen Wang, Muyi Yang","doi":"10.1166/jbn.2023.3717","DOIUrl":"https://doi.org/10.1166/jbn.2023.3717","url":null,"abstract":"We investigated the role of circ_0132269 in hepatocellular carcinoma (HCC). We examined circ_0132269 levels in HCC tissues and cell lines using qRT-PCR. Survival analysis was performed to assess the correlation between circ_0132269 expression and HCC patient survival rates. Knockdown\u0000 of circ_0132269 was performed to evaluate its impact on HCC cell proliferation, migration, and invasion. Bioinformatics analysis predicted that circ_0132269 could interact with miR-1248. This interaction was confirmed using dual luciferase assays, and the correlation between circ_0132269 and\u0000 miR-1248 was analyzed. Further functional experiments investigated the effect of miR-1248 on circ_0132269-mediated malignant phenotypes. circ_0132269 was significantly upregulated in HCC tissues and cell lines. Higher circ_0132269 expression correlated with poorer overall and disease-free\u0000 survival in HCC patients. Silencing circ_0132269 suppressed HCC cell proliferation, migration, and invasion. Bioinformatics analysis revealed a binding site between circ_0132269 and miR-1248. miR-1248 expression was reduced in HCC, while its target MTO1 was highly expressed. miR-1248 levels\u0000 showed a negative correlation with circ_0132269 and MTO1 levels, while circ_0132269 and MTO1 exhibited a positive correlation. Overexpression of miR-1248 partially reversed the promotive effect of highly expressed circ_0132269 on HCC cell behaviors. circ_0132269 was significantly upregulated\u0000 in HCC and associated with poor prognosis. It interacts with miR-1248 to regulate HCC malignancy, highlighting its potential as a diagnostic and therapeutic target.","PeriodicalId":15260,"journal":{"name":"Journal of biomedical nanotechnology","volume":" 5","pages":""},"PeriodicalIF":2.9,"publicationDate":"2023-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138612780","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}
We aimed to study the factors influencing the extent of anterior talofibular ligament (ATFL) and calcaneal ligament (CFL) injuries in acute ankle fractures based on construction of an Artificial Neural Network (ANN) Model. Differences in various baseline data, including personal data, anthropometric data, disease history, and life history, were compared among patients with ATFL injury, ATFL+CFL injury, and ATFL fracture. Factors influencing the ATFL injury/ATFL+CFL injury/ATFL fracture were analyzed using logistic regression, and an artificial neural network (ANN) model for predicting ATFL fracture was constructed using the tensor flow framework. Advanced age (OR= 36.33, 95%CI (15.72, 60.62)), male (OR = 21.21, 95%CI (5, 39.92)), high BMI (OR = 0.03, 95%CI (−0.31 0.37)), exercise duration (OR = 0.48, 95%CI (−14.66, 18.3)), and history of diabetes (OR = 16.98, 95%CI (−76.44, 480.78)) may all be influential factors in the ATFL and CFL injury/ATFL rupture. We constructed three neural layers, the first containing 11 ganglia, the second containing 7 ganglia, and the third containing 5 ganglia, and after 10 iterations the ANN model LOSS values were reduced to the lowest and scatter plots were made of the true and predicted values with some linear trend and better prediction. Advanced age, male, high BMI, length of exercise, and history of diabetes may be influential factors in the ATFL and CFL injuries/ATFL rupture. Applying the tensor flow framework, the ANN algorithm was constructed to predict the occurrence of ATFL fracture with good results.
{"title":"Construction of an Artificial Neural Network Model for Predicting Ankle Ligament Injury Based on the Results of Ultrasonic Shear Wave Technology and Magnetic Resonance Imaging","authors":"Jiong Zhang, Ying Zhao, Yue Zheng, Qinmao Fang, Xin He, Guowei Ren","doi":"10.1166/jbn.2023.3714","DOIUrl":"https://doi.org/10.1166/jbn.2023.3714","url":null,"abstract":"We aimed to study the factors influencing the extent of anterior talofibular ligament (ATFL) and calcaneal ligament (CFL) injuries in acute ankle fractures based on construction of an Artificial Neural Network (ANN) Model. Differences in various baseline data, including personal data,\u0000 anthropometric data, disease history, and life history, were compared among patients with ATFL injury, ATFL+CFL injury, and ATFL fracture. Factors influencing the ATFL injury/ATFL+CFL injury/ATFL fracture were analyzed using logistic regression, and an artificial neural network (ANN) model\u0000 for predicting ATFL fracture was constructed using the tensor flow framework. Advanced age (OR= 36.33, 95%CI (15.72, 60.62)), male (OR = 21.21, 95%CI (5, 39.92)), high BMI (OR = 0.03, 95%CI (−0.31 0.37)), exercise duration (OR = 0.48, 95%CI (−14.66, 18.3)), and history of diabetes\u0000 (OR = 16.98, 95%CI (−76.44, 480.78)) may all be influential factors in the ATFL and CFL injury/ATFL rupture. We constructed three neural layers, the first containing 11 ganglia, the second containing 7 ganglia, and the third containing 5 ganglia, and after 10 iterations the ANN model\u0000 LOSS values were reduced to the lowest and scatter plots were made of the true and predicted values with some linear trend and better prediction. Advanced age, male, high BMI, length of exercise, and history of diabetes may be influential factors in the ATFL and CFL injuries/ATFL rupture.\u0000 Applying the tensor flow framework, the ANN algorithm was constructed to predict the occurrence of ATFL fracture with good results.","PeriodicalId":15260,"journal":{"name":"Journal of biomedical nanotechnology","volume":" 2","pages":""},"PeriodicalIF":2.9,"publicationDate":"2023-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138615593","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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