Chinese Journal of Physiology最新文献

{"title":"Sericin improves memory and sociability impairments evoked by transient global cerebral ischemia through suppression of hippocampal oxidative stress, inflammation, and apoptosis.","authors":"Seyed Mehdi Vatandoust,&nbsp;Javad Mahmoudi,&nbsp;Shahrbanoo Oryan,&nbsp;Fereshteh Farajdokht,&nbsp;Saeed Sadigh-Eteghad,&nbsp;Siamak Sandoghchian Shotorbani,&nbsp;Huaxi Xu,&nbsp;Delaram Eslimi Esfahani","doi":"10.4103/cjop.CJOP-D-23-00006","DOIUrl":"10.4103/cjop.CJOP-D-23-00006","url":null,"abstract":"<p><p>Sericin (Ser) is a natural neuroactive macromolecule with diverse pharmacological properties, and our previous findings have shown its neuroprotective potentials. This study aimed to investigate the therapeutic potential of Ser on cognitive dysfunction induced by transient global cerebral ischemia/reperfusion (tGI/R) and its mechanism of action. The tGI/R was induced in BALB/c mice by bilateral occlusion of the common carotid arteries for two 5 min followed by a 10-min reperfusion period. After 24 h, mice were treated with normal saline or different doses of Ser (100, 200, and 300 mg/kg) for 10 days. Cognitive performances were assessed using the Barnes maze and social interaction tasks. Oxidative stress markers including superoxide dismutase (SOD), glutathione peroxidase (GPx), total antioxidant capacity (TAC), and malondialdehyde (MDA) as well as pro-inflammatory cytokines (interleukin (IL)-6 and tumor necrosis factor-alpha) and anti-inflammatory cytokine (IL-10) were assessed in the hippocampus. Markers of apoptosis (pro- and cleaved caspase-9 and 3, Bax, and Bcl-2) were assessed by Western blotting. Besides, transferase-mediated dUTP nick end-labeling assay was used to detect apoptotic cell death. We show here that Ser administration improved tGI/R-induced cognitive deficits, enhanced the activity of SOD and GPx, increased TAC levels, while reduced MDA levels. Notably, Ser decreased neuronal apoptotic cell death in the hippocampal dentate gyrus (DG) region, accompanied by suppression of neuroinflammation, downregulation of pro-apoptotic proteins (caspase-9, caspases-3, and Bax), and upregulation of anti-apoptotic protein, Bcl-2. Taken together, Ser administration protected hippocampal neurons from apoptotic cell death by impeding oxidative stress and inflammatory responses and, in turn, improved cognitive function in the tGI/R mice.</p>","PeriodicalId":10251,"journal":{"name":"Chinese Journal of Physiology","volume":null,"pages":null},"PeriodicalIF":1.8,"publicationDate":"2023-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10459230","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}

{"title":"Ring-finger protein 5 attenuates oxygen-glucose deprivation and reperfusion-induced mitochondrial dysfunction and inflammation in cardiomyocytes by inhibiting the S100A8/MYD88/NF-κB axis.","authors":"Xuesi Chen,&nbsp;Yingjie Wu,&nbsp;Yingchun Bao","doi":"10.4103/cjop.CJOP-D-22-00140","DOIUrl":"10.4103/cjop.CJOP-D-22-00140","url":null,"abstract":"<p><p>Mitochondrial dysfunction is closely intertwined with the progression of heart failure (HF). Ring-finger protein 5 (RNF5) is an E3 ubiquitin ligase, whose deletion induces the enhanced S100A8 expression. S100A8 regulates the mitochondrial dysfunction and S100A8/myeloid differentiation factor 88 (MYD88)/nuclear factor-kappa B (NF-κB) pathway promotes an inflammatory response; however, whether RNF5 modulated mitochondrial dysregulation and inflammation through the S100A8/MYD88/NF-κB axis remains unknown. Here, H9c2 cells were stimulated with oxygen-glucose deprivation/reperfusion (OGD/R) to build a HF model in vitro. RNF5 level was assessed in gene expression omnibus database and in OGD/R-induced H9c2 cells with reverse transcriptase quantitative polymerase chain reaction and western blot. The RNF5 level was overexpressed via transfecting RNF5 overexpression plasmids into H9c2 cells. The role and mechanism of RNF5 in OGD/R-elicited H9c2 cells were determined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide, spectrophotometry, flow cytometry, mitochondrial membrane potential (MMP) measurement, enzyme-linked immunosorbent assay and western blot assays. The RNF5 expression was downregulated both in silico and in OGD/R-stimulated H9c2 cells. OGD/R treatment caused a decrease in the cell viability, the MMP level, and the translational expression of mito-cyt-c and NF-κB-cyto, and an elevation in the concentrations of lactate dehydrogenase and creatine kinase myocardial band, the apoptosis rate, the inflammatory factor release, and the relative protein expression of cyto-cyt-c, S100A8, MYD88 and NF-κB-nuc in H9c2 cells. Upregulation of RNF5 reversed these indicators in OGD/R-stimulated H9c2 cells. Altogether, based on these outcomes, we concluded that RNF5 impeded mitochondrial dysfunction and inflammation through attenuating the S100A8/MYD88/NF-κB axis in OGD/R-stimulated H9c2 cells.</p>","PeriodicalId":10251,"journal":{"name":"Chinese Journal of Physiology","volume":null,"pages":null},"PeriodicalIF":1.8,"publicationDate":"2023-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10459233","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}

{"title":"Investigation of the regulatory mechanism of lijie capsules on gut microbiota in rheumatoid arthritis.","authors":"Yanqiang Chen,&nbsp;Shaobin Qiu,&nbsp;Fei Qiu,&nbsp;Guoyuan Li,&nbsp;Lixian Gan,&nbsp;Binghui Huang,&nbsp;Lingmei Yang","doi":"10.4103/cjop.CJOP-D-22-00134","DOIUrl":"10.4103/cjop.CJOP-D-22-00134","url":null,"abstract":"<p><p>Lijie Capsules (LJJN) are a classical Chinese herbal formula adopted to treat rheumatoid arthritis (RA) clinically, yet the regulatory mechanism underlying the protection of LJJN against RA has not been fully elucidated. Here, the animal model of RA was established by complete Freund's adjuvant administration in mice. About 60 mg/ml of LJJN was used for treatment. The histological change of ankle joint was measured by hematoxylin and eosin staining. The inflammatory cytokines were detected using ELISA kits. The protein associated with inflammation and GLUD2 was detected using Western blot. The mice feces were analyzed by 16S rRNA sequencing. The levels of glutamate (Glu) and α-ketoglutarate (α-KG) were detected using their detection kits. In addition, fibroblast-like synoviocytes (FLSs) were stimulated by Glu to induce an injured synoviocytes model in vitro, with or without LJJN treatment for 48 h. It was demonstrated that LJJN alleviated ankle joint swelling and synovial injury in RA mice. Meanwhile, LJJN inactivated nuclear factor kappa B signaling and suppressed inflammation of RA mice. The disordered gut microbiota composition in RA mice was partly restored by LJJN. Bacteroides-mediated Glu metabolism was impacted in RA mice, and LJJN contributed to the conversion of Glu to α-KG in RA mice. In addition, the in vitro results revealed that LJJN could block Glu-induced inflammation in FLSs but had no direct influence on α-KG and GLUD2 levels. In summary, LJJN exerted a protective role against ankle joint injury and inflammation in RA, which might be partly associated with gut microbiota-mediated Glu metabolism.</p>","PeriodicalId":10251,"journal":{"name":"Chinese Journal of Physiology","volume":null,"pages":null},"PeriodicalIF":1.8,"publicationDate":"2023-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10459232","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}

{"title":"E2F8 knockdown suppresses cell proliferation and induces cell cycle arrest via Wnt/β-Catenin pathway in ovarian cancer.","authors":"Meiyin Zhang,&nbsp;Ye Xu,&nbsp;Yongjian Zhang,&nbsp;Ge Lou","doi":"10.4103/cjop.CJOP-D-22-00142","DOIUrl":"10.4103/cjop.CJOP-D-22-00142","url":null,"abstract":"<p><p>Ovarian cancer is one of the leading causes of death in female reproductive system cancers. However, the pathogenesis of ovarian cancer remains elusive. Our aim is to investigate the potential targets for ovarian cancer. Two microarray datasets were obtained from the Gene Expression Omnibus public database. Using R package limma, the differentially expressed genes (DEGs) were identified from the datasets. There were 95 overlapping DEGs in two microarray datasets. GO, KEGG pathway analysis, and protein-protein interaction (PPI) network analysis were carried out based on the DEGs. Wnt signaling pathway and cell cycle were enriched in the KEGG pathway analysis. Moreover, the top 10 hub genes with the most nodes were determined by PPI network analysis. E2F8, one of hub genes was positively linked to a bad outcome in ovarian cancer patients. Furthermore, E2F8 knockdown suppressed cell proliferation and induced cell cycle arrest in ovarian cancer. In addition, we found that silencing E2F8 inhibited the Wnt/β-catenin signaling pathway. In ovarian cancer cells with E2F8 knockdown, overexpressing β-catenin restored both the suppressed capacity of cell proliferation and cell cycle progression. Therefore, our results revealed that E2F8 had an involvement in the development of ovarian cancer which might act as a therapeutic target.</p>","PeriodicalId":10251,"journal":{"name":"Chinese Journal of Physiology","volume":null,"pages":null},"PeriodicalIF":1.8,"publicationDate":"2023-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10139266","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}

{"title":"Genkwanin suppresses mitochondrial dysfunction to alleviate IL-1β-elicited inflammation, apoptosis, and degradation of extracellular matrix in chondrocytes through upregulating DUSP1.","authors":"Kanna Xu,&nbsp;Haoran Wang,&nbsp;Zhongqing Wu","doi":"10.4103/cjop.CJOP-D-23-00031","DOIUrl":"10.4103/cjop.CJOP-D-23-00031","url":null,"abstract":"<p><p>Osteoarthritis (OA) is a form of chronic degenerative disease contributing to elevated disability rate among the elderly. Genkwanin is an active component extracted from Daphne genkwa possessing pharmacologic effects. Here, this study is designed to expound the specific role of genkwanin in OA and elaborate the probable downstream mechanism. First, the viability of chondrocytes in the presence or absence of interleukin-1 beta (IL-1β) treatment was detected by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay. Terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling assay was used to assess cell apoptosis. Inflammatory response was estimated through enzyme-linked immunosorbent assay and Western blot. In addition, immunofluorescence staining and Western blot were utilized to measure the expression of extracellular matrix (ECM)-associated proteins. Dual-specificity protein phosphatase-1 (DUSP1) expression was tested by reverse transcription-quantitative polymerase chain reaction (RT-qPCR) and Western blot. Following DUSP1 elevation in genkwanin-treated chondrocytes exposed to IL-1β, inflammatory response and ECM-associated factors were evaluated as forementioned. In addition, 5,5',6,6'-tetrachloro-1,1',3,3'-tetraethylbenzimidazolocarbocyanine iodide staining was to assess the mitochondrial membrane potential. Adenosine triphosphate (ATP) level was examined with ATP assay kit, and RT-qPCR was used to test mitochondrial DNA expression. Results indicated that genkwanin administration enhanced the viability while ameliorated the apoptosis, inflammatory response, and ECM degradation in IL-1β-induced chondrocytes. Besides, genkwanin treatment fortified DUSP1 expression in IL-1β-exposed chondrocytes. DUSP1 interference further offsets the impacts of genkwanin on the inflammation, ECM degradation, and mitochondrial dysfunction in IL-1β-challenged chondrocytes. In short, genkwanin enhanced DUSP1 expression to mitigate mitochondrial dysfunction, thus ameliorating IL-1β-elicited inflammation, apoptosis, and degradation of ECM in chondrocytes.</p>","PeriodicalId":10251,"journal":{"name":"Chinese Journal of Physiology","volume":null,"pages":null},"PeriodicalIF":1.8,"publicationDate":"2023-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10439700","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}

{"title":"Stomatin-like protein-2 contributes the migration and invasion of breast cancer cells via regulating ERK/FOXO3a signaling pathway.","authors":"Shengming Wu,&nbsp;Lingang Zhao,&nbsp;Qian Li","doi":"10.4103/cjop.CJOP-D-22-00117","DOIUrl":"10.4103/cjop.CJOP-D-22-00117","url":null,"abstract":"<p><p>Breast cancer (BC) is the most common tumor in women, and its incidence is increasing, ranking first among female malignant tumors. It is urgently needed to find new and reliable biomarkers of BC and to understand the cellular changes that cause metastasis. Stomatin-like protein-2 (SLP-2) is a member of the stomatin protein superfamily. Studies have shown that SLP-2 was highly expressed in some tumors and played an important role in tumor genesis and development. SLP-2 regulated the extracellular signal-regulated kinase (ERK) pathway, and activation of ERK phosphorylated FOXO3a, which was involved in BC progression. However, its possible role in the progression of BC remains unclear. In this study, we found the high expression of SLP-2 in BC tissues and cells. SLP-2 promoted the viability of BC cells. In addition, we found that SLP-2 stimulated the motility of BC cells in vitro. Mechanically, our results revealed that SLP-2 could mediate FOXO3a expression and ERK signaling pathway, thereby contributing to the viability and motility of BC cells. Therefore, SLP-2 has the potential to serve as a promising target for BC treatment.</p>","PeriodicalId":10251,"journal":{"name":"Chinese Journal of Physiology","volume":null,"pages":null},"PeriodicalIF":1.8,"publicationDate":"2023-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10439696","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}

{"title":"Pachymic acid protects hepatic cells against oxygen-glucose deprivation/reperfusion injury by activating sirtuin 1 to inhibit HMGB1 acetylation and inflammatory signaling.","authors":"Chengbiao Xue,&nbsp;Zhigao Xu,&nbsp;Zhongzhong Liu,&nbsp;Cheng Zeng,&nbsp;Qifa Ye","doi":"10.4103/cjop.CJOP-D-22-00118","DOIUrl":"10.4103/cjop.CJOP-D-22-00118","url":null,"abstract":"<p><p>Ischemia-reperfusion injury is an important cause of liver injury occurring during liver transplantation. It is usually caused by inflammatory response and oxidative stress-induced oxidative damage. Pachymic acid (PA) has various biological activities such as anti-inflammatory, antioxidant and anti-cancer. However, the action mechanism of PA in hepatic ischemia-reperfusion injury is currently unknown. In this study, liver cells were subjected to oxygen-glucose deprivation/reperfusion (OGD/R) to simulate a hepatic ischemia-reperfusion injury model. The binding relationship between PA and sirtuin 1 (SIRT1) was analyzed by molecular docking. Cell viability was detected by Cell Counting Kit-8. Expression levels of SIRT1 and high mobility group box 1 (HMGB1) were detected by western blot. Subsequent levels of inflammatory factors were detected by related kits and western blot. Meanwhile, related kits were used to examine levels of oxidative stress markers including reactive oxygen species, malondialdehyde, superoxide dismutase and cytotoxicity-associated lactate dehydrogenase. Finally, cell apoptosis was detected by flow cytometry and western blot. The results showed that PA significantly ameliorated OGD/R-induced decrease in SIRT1 expression, increase in HMGB1 acetylation and HMGB1 translocation. Moreover, the elevated levels of inflammatory factors, oxidative stress indexes and cell apoptosis upon exposure to OGD/R were reversed by PA treatment. Moreover, the addition of SIRT1 agonist and inhibitor further demonstrated that PA exerted the aforementioned effects in OGD/R-exposed cells by targeting SIRT1. Thus, the present study revealed the mechanism by which PA ameliorated OGD/R-induced hepatic injury via SIRT1. These results might provide a clearer theoretical basis for the targeted treatment of OGD/R-induced hepatic injury with PA.</p>","PeriodicalId":10251,"journal":{"name":"Chinese Journal of Physiology","volume":null,"pages":null},"PeriodicalIF":1.8,"publicationDate":"2023-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10439698","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}

{"title":"Paeonol represses A549 cell glycolytic reprogramming and proliferation by decreasing m6A modification of Acyl-CoA dehydrogenase.","authors":"Lixin Zhang,&nbsp;Lihua Wu,&nbsp;Xiangrui Zhu,&nbsp;Jian Mei,&nbsp;Yingli Chen","doi":"10.4103/cjop.CJOP-D-22-00166","DOIUrl":"10.4103/cjop.CJOP-D-22-00166","url":null,"abstract":"<p><p>Aberrant glycolytic reprogramming is involved in lung cancer progression by promoting the proliferation of non-small cell lung cancer cells. Paeonol, as a traditional Chinese medicine, plays a critical role in multiple cancer cell proliferation and inflammation. Acyl-CoA dehydrogenase (ACADM) is involved in the development of metabolic diseases. N6-methyladenosine (m6A) modification is important for the regulation of messenger RNA stability, splicing, and translation. Here, we investigated whether paeonol regulates the proliferation and glycolytic reprogramming via ACADM with m6A modification in A549 cells (human non-small cell lung cancer cells). Cell counting kit 8, 5-Bromo-2-deoxyuridine, 5-ethynyl-2'-deoxyuridine (EdU) incorporation, flow cytometry analysis, western blotting and seahorse XFe24 extracellular flux analyzer assays showed that paeonol had a significant inhibitory effect against A549 cell proliferation and glycolysis. Mechanistically, ACADM was a functional target of paeonol. We also showed that the m6A reader YTH domain containing 1 plays an important role in m6A-modified ACADM expression, which is negatively regulated by paeonol, and is involved in A549 cell proliferation and glycolytic reprogramming. These results indicated the central function of paeonol in regulating A549 cell glycolytic reprogramming and proliferation via m6A modification of ACADM.</p>","PeriodicalId":10251,"journal":{"name":"Chinese Journal of Physiology","volume":null,"pages":null},"PeriodicalIF":1.8,"publicationDate":"2023-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10439699","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}

{"title":"LSD1 silencing inhibits the proliferation, migration, invasion, and epithelial-to-mesenchymal transition of hypopharyngeal cancer cells by inducing autophagy and pyroptosis.","authors":"Hao Wang,&nbsp;Fang Liu","doi":"10.4103/cjop.CJOP-D-22-00137","DOIUrl":"https://doi.org/10.4103/cjop.CJOP-D-22-00137","url":null,"abstract":"<p><p>Hypopharyngeal cancer is a subtype of the head and neck malignancies. We aimed to explore the role of lysine-specific demethylase 1 (LSD1/KDM1A) in the progression of hypopharyngeal cancer and to identify the potential mechanisms. First, LSD1 expression in head and neck squamous cell carcinoma (HNSCC) tissues and the correlation between LSD1 and the stage of HNSC were analyzed by the University of ALabama at Birmingham CANcer data analysis Portal (UALCAN). Following LSD1 silencing, proliferation of pharyngeal cancer cell line FaDu cells was evaluated by cell counting kit-8 and colony formation assays. Wounding healing and transwell assays were used to measure the capacities of migration and invasion. In addition, expression of proteins related to epithelial-to-mesenchymal transition (EMT), autophagy, and pyroptosis was tested by Western blot analysis or immunofluorescence. After treatment with autophagy inhibitor 3-methyladenine (3-MA) or NLR family pyrin domain containing 3 (NLRP3) inhibitor MCC950, the malignant biological properties were measured again. High LSD1 expression was observed in HNSC tissues, which was correlated with stage. LSD1 knockdown significantly suppressed the proliferation, migration, invasion, and EMT of hypopharyngeal cancer cells. Moreover, autophagy and pyroptosis were induced by LSD1 depletion, observed by the enhanced fluorescence intensity of LC3, gasdermin-D (GSDMD)-N, and apoptosis-associated speck-like protein containing a CARD (ASC), accompanied by upregulated expression of LC3II/LC3I, Beclin-1, NLRP3, cleaved-caspase 1, ASC, interleukin (IL)-1β, and IL-18 and downregulated expression of p62. Importantly, 3-MA or MCC950 addition obviously reversed the inhibitory effects of LSD1 silencing on the proliferation, migration, invasion, and EMT of hypopharyngeal cancer cells. To sum up, LSD1 silencing could restrain the progression of hypopharyngeal cancer cells by inducing autophagy and pyroptosis.</p>","PeriodicalId":10251,"journal":{"name":"Chinese Journal of Physiology","volume":null,"pages":null},"PeriodicalIF":1.8,"publicationDate":"2023-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9655766","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}

{"title":"L-limonene reduces aortic artery atherosclerosis by inhibiting oxidative stress/inflammatory responses in diabetic rats fed high-fat diet.","authors":"Xia Han,&nbsp;Huaxin Qi,&nbsp;Jiamin Niu","doi":"10.4103/cjop.CJOP-D-22-00139","DOIUrl":"https://doi.org/10.4103/cjop.CJOP-D-22-00139","url":null,"abstract":"<p><p>Atherosclerosis, a leading cause of mortality worldwide, is driven by multiple risk factors such as diabetes. Oxidative stress and inflammation assist interrelated roles in diabetes-accelerated atherosclerosis. Thereby, treatment of diabetic atherosclerosis from an oxidative stress/inflammatory perspective seems to be a more effective modality to prevent and delay plaque formation and progression. This study aimed to evaluate the effects of l-limonene (LMN) on oxidative stress/inflammatory responses in the aortic artery of diabetic atherosclerosis-modeled rats. Male Wistar rats (n = 30, 250-280 g, 12 weeks old) were used to establish a diabetic atherosclerosis model (8 weeks) using high-fat diet/low-dose streptozotocin. LMN (200 mg/kg/day) was administered orally, starting on day 30^th before tissue sampling. Plasma lipid profiles, aortic histopathological changes, atherogenic index, aortic artery levels of oxidative stress markers (manganese superoxide dismutase, glutathione, and 8-isoprostane), inflammatory markers (tumor necrosis factor-alpha, interleukin (IL)-6, and IL-10), and expression of phosphorylated adenosine monophosphate-activated protein kinase (p-AMPK)/AMPK, Sirtuin 1 (SIRT1), and p-p65/p65 proteins were evaluated. The administration of LMN to diabetic rats improved lipid profiles, aortic histopathological morphology, and atherogenic index (P < 0.05 to P < 0.001). It also increased enzymatic antioxidant activities, decreased 8-isoprostane level, suppressed inflammatory response, upregulated p-AMPK and SIRT1 proteins, and downregulated p-p65 protein (P < 0.05 to P < 0.01). Inhibiting the AMPK through the administration of compound C significantly abolished or reversed the positive effects of LMN in diabetic rats (P < 0.05 to P < 0.01). LMN treatment had dual anti-oxidative and anti-inflammatory actions against atherosclerosis in the aortic artery of diabetic rats. Atheroprotection by LMN was mediated partly through modulation of AMPK/SIRT1/p65 nuclear factor kappa B signaling pathway. LMN appears to be a promising anti-atherosclerotic modality to improve the quality of life in diabetic patients.</p>","PeriodicalId":10251,"journal":{"name":"Chinese Journal of Physiology","volume":null,"pages":null},"PeriodicalIF":1.8,"publicationDate":"2023-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9708971","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}