General physiology and biophysics最新文献_第2页

Platelet-rich fibrin combined with naringin accelerates diabetic wound healing by enhancing re-epithelialization and reducing inflammation. 富血小板纤维蛋白联合柚皮苷通过增强再上皮化和减少炎症加速糖尿病伤口愈合。

IF 1.5 4区生物学

General physiology and biophysics Pub Date : 2026-07-01 DOI: 10.4149/gpb_2026010

Huan Tong, Hu Gao, Jing Zeng, Rong Liang, Xiangming Zhang

{"title":"Platelet-rich fibrin combined with naringin accelerates diabetic wound healing by enhancing re-epithelialization and reducing inflammation.","authors":"Huan Tong, Hu Gao, Jing Zeng, Rong Liang, Xiangming Zhang","doi":"10.4149/gpb_2026010","DOIUrl":"10.4149/gpb_2026010","url":null,"abstract":"Delayed wound healing, one of the fatal complications that affect about 15% of diabetic patients, is associated with impaired keratinocyte proliferation and migration and enhanced inflammation. In this research, we investigated the combined application of platelet-rich fibrin (PRF) and the natural flavonoid naringin for wound healing in diabetic conditions. High glucose (HG)-stimulated human keratinocytes HaCaT and high fat diet + streptozotocin-induced diabetic rats were treated with PRF and naringin alone or in combination. HaCaT cell proliferation and migration were detected by EdU staining and wound healing assay. On days 0, 3, 7, and 14 after wound creation, the wound healing rates in diabetic rats were calculated. The combined treatment of PRF and naringin was more effective than PRF or naringenin alone in enhancing cell proliferation and migration and attenuating MMP2/9 and pro-inflammatory cytokine expression in HG-exposed HaCaT cells. PRF and naringin combination exhibited higher efficacy in accelerating wound closure, elevating cell proliferation, and reducing inflammation and NF-κB phosphorylation in rat wound tissues vs. PRF or naringin treatment alone. In conclusion, the combined treatment of PRF and naringin is more effective than either treatment alone in promoting the healing of diabetic wounds through enhancing wound re-epithelialization and alleviating inflammation.","PeriodicalId":12514,"journal":{"name":"General physiology and biophysics","volume":"45 4","pages":"351-363"},"PeriodicalIF":1.5,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148711885","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Calycosin ameliorates airway inflammatory injury induced by respiratory syncytial virus via inhibiting NLRP3 inflammasome activation in mice. 毛蕊异黄酮通过抑制NLRP3炎性体激活改善呼吸道合胞病毒诱导的小鼠气道炎症损伤。

IF 1.5 4区生物学

General physiology and biophysics Pub Date : 2026-07-01 DOI: 10.4149/gpb_2026016

Xuan Wang, Shanxia Wu, Heng Jiang, Hong Jiang

{"title":"Calycosin ameliorates airway inflammatory injury induced by respiratory syncytial virus via inhibiting NLRP3 inflammasome activation in mice.","authors":"Xuan Wang, Shanxia Wu, Heng Jiang, Hong Jiang","doi":"10.4149/gpb_2026016","DOIUrl":"https://doi.org/10.4149/gpb_2026016","url":null,"abstract":"Respiratory syncytial virus (RSV) is a predominant pathogen inducing respiratory tract infections among infants and elderly. Calycosin exhibits antiviral properties, yet its efficacy against RSV has not been elucidated. In this study, cyclophosphamide was administered to induce immune deficiency in adult mice, following which RSV was introduced via the intranasal route to establish an RSV infection model in mice. The viral load in lung tissue, airway resistance, inflammatory cell quantity and pro-inflammatory factor levels within bronchoalveolar lavage fluid (BALF) were quantified. Pathological changes were examined and the NOD-like receptor protein 3 (NLRP3) inflammasome activation status was assessed in lung tissue. The results demonstrated that Calycosin treatment markedly decreased the RSV viral load inside lung tissue, decreased inflammatory factor quantity and pro-inflammatory factor levels within BALF, and alleviated airway resistance, inflammatory injury, as well as goblet cell hyperplasia of mouse lung tissue. Notably, Calycosin significantly suppressed NLRP3 inflammasome activation inside RSV-infected mouse lung tissue. However, co-treatment with Nigericin diminished the protective effects of Calycosin on airway inflammatory injury in RSV-infected mice. These findings indicate that Calycosin alleviates airway injury induced by RSV infection, and the underlying mechanism is associated with the inhibition of the inflammatory response mediated by NLRP3 inflammasome activation.","PeriodicalId":12514,"journal":{"name":"General physiology and biophysics","volume":"45 4","pages":"365-374"},"PeriodicalIF":1.5,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148711906","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Phloretin alleviates renal injury in streptozotocin-induced diabetic mice through NF-κB/MAPK signaling pathways. 根皮素通过NF-κB/MAPK信号通路减轻链脲佐菌素诱导的糖尿病小鼠肾损伤。

IF 1.5 4区生物学

General physiology and biophysics Pub Date : 2026-07-01 DOI: 10.4149/gpb_2026013

Xiaoshan Xu, Chunshui Gong, Xiaoyan Bian

{"title":"Phloretin alleviates renal injury in streptozotocin-induced diabetic mice through NF-κB/MAPK signaling pathways.","authors":"Xiaoshan Xu, Chunshui Gong, Xiaoyan Bian","doi":"10.4149/gpb_2026013","DOIUrl":"https://doi.org/10.4149/gpb_2026013","url":null,"abstract":"Diabetic nephropathy (DN) is a complication of diabetes characterized by renal dysfunction, fibrosis, and inflammation. This study aimed to investigate the nephroprotective effects of phloretin (PHL) in a streptozotocin (STZ)-induced diabetic mouse model. Mice were treated with PHL (50 mg/kg/day) for eight weeks, after which renal function parameters, oxidative stress markers, histopathological changes, fibrosis- and inflammation-related protein expression, and key signaling pathways were analyzed. The results demonstrated that PHL ameliorated hyperglycemia, renal dysfunction (as evidenced by reduced BUN, serum creatinine, and urinary albumin), and dyslipidemia (lowered serum TG and TC). PHL also attenuated renal oxidative stress by enhancing antioxidant enzyme activities (SOD, CAT, GSH-Px) and reducing lipid peroxidation (MDA). Histopathological evaluation revealed that PHL alleviated glomerular damage, tubular necrosis, and inflammatory cell infiltration, while Masson's staining showed inhibition of renal interstitial fibrosis. Mechanistically, PHL downregulated the expression of fibrosis markers (fibronectin, collagen I, α-SMA) and proinflammatory cytokines (IL-6, IL-1β, TNF-α). Furthermore, PHL suppressed the activation of the NF-κB and MAPK pathways, as indicated by increased IκBα levels and reduced phosphorylation of NF-κB p65, p38, JNK, and ERK1/2. In conclusion, PHL protects against DN by improving renal function, reducing oxidative stress, mitigating fibrosis and inflammation, and inactivating the NF-κB/MAPK pathways.","PeriodicalId":12514,"journal":{"name":"General physiology and biophysics","volume":"45 4","pages":"397-407"},"PeriodicalIF":1.5,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148711950","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

SWAP70 alleviates brain damage and neuroinflammation induced by cerebral ischemia-reperfusion by inhibiting autophagy. SWAP70通过抑制自噬减轻脑缺血再灌注引起的脑损伤和神经炎症。

IF 1.5 4区生物学

General physiology and biophysics Pub Date : 2026-07-01 DOI: 10.4149/gpb_2026017

Yu Shi, Fangfang Hu, Zhengdong Li, Ke Xu

{"title":"SWAP70 alleviates brain damage and neuroinflammation induced by cerebral ischemia-reperfusion by inhibiting autophagy.","authors":"Yu Shi, Fangfang Hu, Zhengdong Li, Ke Xu","doi":"10.4149/gpb_2026017","DOIUrl":"https://doi.org/10.4149/gpb_2026017","url":null,"abstract":"Cerebral ischemia-reperfusion (CIR) injury is a leading cause of neurological disability and is characterized by oxidative stress, inflammation, and excessive autophagy, all of which converge to promote neuronal injury and death. Autophagy plays a dual role in this setting by helping to maintain cellular homeostasis under stress, yet it can drive neurodegeneration when overactivated. Switch-associated protein 70 (SWAP70), a Rho GTPase exchange factor that regulates cytoskeletal dynamics and immune responses, has been implicated in neural differentiation and inflammatory regulation; however, its role in CIR injury remains unclear. In this study, using middle cerebral artery occlusion/reperfusion (MCAO/R) mice and oxygen-glucose deprivation/reoxygenation (OGD/R)-treated SH-SY5Y cells, we found that SWAP70 expression was significantly reduced after ischemic injury. Notably, SWAP70 overexpression improved neurological function and reduced infarct size, neuronal damage, and cytokine release in MCAO/R mice. Consistently, in OGD/R-treated SH-SY5Y cells, SWAP70 overexpression restored cell viability, decreased LDH release, and suppressed the expression of autophagy-related proteins. Importantly, rapamycin treatment reversed the protective effects of SWAP70, confirming that SWAP70 alleviates brain injury by inhibiting excessive autophagy. Furthermore, SWAP70 overexpression suppressed NF-κB pathway activation. In conclusion, SWAP70 mitigates CIR injury by inhibiting excessive autophagy and dampening neuroinflammation, thereby providing a potential therapeutic target for ischemic stroke.","PeriodicalId":12514,"journal":{"name":"General physiology and biophysics","volume":"45 4","pages":"387-395"},"PeriodicalIF":1.5,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148711970","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

From SHP2 to DDR1-ERK: A critical signaling axis controlling microglial activation and neuropathic pain after spinal cord injury. 从SHP2到DDR1-ERK：脊髓损伤后控制小胶质细胞激活和神经性疼痛的关键信号轴

IF 1.5 4区生物学

General physiology and biophysics Pub Date : 2026-07-01 DOI: 10.4149/gpb_2026009

Wei Zhang, Zhenwei Xu

{"title":"From SHP2 to DDR1-ERK: A critical signaling axis controlling microglial activation and neuropathic pain after spinal cord injury.","authors":"Wei Zhang, Zhenwei Xu","doi":"10.4149/gpb_2026009","DOIUrl":"https://doi.org/10.4149/gpb_2026009","url":null,"abstract":"This study explores the role of the src homology-2domain-containing protein tyrosine phosphatase-2 (SHP2)-discoid domain receptor 1 (DDR1)-extracellular signal-regulated kinase (ERK) signaling axis in neuropathic pain following spinal cord injury (SCI). Rats were transfected with LV-shSHP2 before SCI modeling. Hind limb function and paw withdrawal threshold were assessed using the Basso-Beattie-Bresnahan (BBB) scale, and Von Frey filaments, respectively. The effects of SHP2 knockdown on microglial activation and DDR1/SHP2/ERK pathway were examined by Western blotting and immunofluorescence. To further validate the regulatory mechanism of SHP2 in SCI, lipopolysaccharide (LPS)-activated BV-2 microglial cells were subjected to SHP2/DDR1 knockdown, or DDR1 overexpression. Results showed that SCI induced motor deficits, mechanical allodynia, and upregulation of spinal SHP2, DDR1, and p-ERK/ERK ratio, alongside microglial activation. These changes were reversed by LV-shSHP2 treatment. In LPS treated BV-2 cells, DDR1 overexpression promoted cell activation and ERK phosphorylation, while counteracting the effects of LV-shSHP2; however, DDR1 knockdown produced the opposite effects. A direct interaction between SHP2 and DDR1 was confirmed. In conclusion, SHP2 knockdown suppresses microglial hyperactivation and alleviates SCI-induced neuropathic pain by downregulating the DDR1-ERK signaling pathway, during which SHP2-DDR1 interaction has been confirmed as a key regulatory mechanism. Targeting this specific interaction axis may offer a novel therapeutic strategy for neuropathic pain management by selectively disrupting microglial activation.","PeriodicalId":12514,"journal":{"name":"General physiology and biophysics","volume":"45 4","pages":"409-418"},"PeriodicalIF":1.5,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148711921","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

How GP96 upregulation shields against COPD: mitigating endoplasmic reticulum stress-induced cellular damage via p38/ERK pathway activation. GP96上调如何预防COPD：通过p38/ERK通路激活减轻内质网应激诱导的细胞损伤

IF 1.5 4区生物学

General physiology and biophysics Pub Date : 2026-07-01 DOI: 10.4149/gpb_2026012

Lei Xue, Yihui Wang, Ting Yang, Wanling Yang, Ying Liu, Jie Tan

{"title":"How GP96 upregulation shields against COPD: mitigating endoplasmic reticulum stress-induced cellular damage via p38/ERK pathway activation.","authors":"Lei Xue, Yihui Wang, Ting Yang, Wanling Yang, Ying Liu, Jie Tan","doi":"10.4149/gpb_2026012","DOIUrl":"https://doi.org/10.4149/gpb_2026012","url":null,"abstract":"Chronic obstructive pulmonary disease (COPD) is closely associated with endoplasmic reticulum stress (ERS). We explored the potential role of Glycoprotein 96 (GP96) in mitigating ERS-induced cellular damage in an in vitro COPD model. Human bronchial epithelial 16HBE cells were exposed to nicotine to establish a COPD model in vitro. The expression of GP96 was manipulated, and the involvement of the extracellular signal-regulated kinase (ERK) signaling pathway was assessed by treatment with the ERK inhibitor PD98059. The effects of GP96 and the p38/ERK pathway on ERS-related markers, apoptosis and its associated proteins, reactive oxygen species (ROS) levels, proinflammatory cytokines, and the activation levels of ERK and p38 were evaluated. Nicotine induced GP96 expression in 16HBE cells. Nicotine also repressed cell viability, and promoted apoptosis, ROS release, expressions of ERS-related markers and pro-inflammatory cytokines levels in 16HBE cells, which were reversed by GP96 overexpression. Besides, nicotine elevated p-ERK/ERK and p-P38/P38 levels in 16HBE cells, which was further enhanced by GP96 overexpression. In contrast, GP96 silencing produced effects opposite to those of GP96 overexpression. The ERK inhibitor PD98059 offset the effects of GP96 overexpression, except for its impact on the p-P38/P38 levels, which remained unaffected. GP96 overexpression inhibits ERS-induced apoptosis, oxidative stress and inflammation in nicotineinduced in vitro COPD model through potentiating ERK activation.","PeriodicalId":12514,"journal":{"name":"General physiology and biophysics","volume":"45 4","pages":"375-386"},"PeriodicalIF":1.5,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148711901","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Risks and benefits of prenatal exposure to antidepressants: Neurobiological mechanisms and clinical evidence. 产前暴露于抗抑郁药的风险和益处：神经生物学机制和临床证据。

IF 1.5 4区生物学

General physiology and biophysics Pub Date : 2026-07-01 Epub Date: 2026-05-22 DOI: 10.4149/gpb_2026014

Hande Özbaşak, Jana Gaburjáková, Reyhaneh Nejati Bervanlou, Matej Račický, Eliyahu Dremencov, Ruslan Paliokha

{"title":"Risks and benefits of prenatal exposure to antidepressants: Neurobiological mechanisms and clinical evidence.","authors":"Hande Özbaşak, Jana Gaburjáková, Reyhaneh Nejati Bervanlou, Matej Račický, Eliyahu Dremencov, Ruslan Paliokha","doi":"10.4149/gpb_2026014","DOIUrl":"10.4149/gpb_2026014","url":null,"abstract":"This review summarizes current evidence on how maternal stress, depression, and antidepressant treatment during pregnancy influence offspring neurodevelopment. We focus on neurobiological mechanisms linking maternal and fetal brains, particularly interactions between monoaminergic systems and the brain-derived neurotrophic factor (BDNF)-tyrosine kinase receptor B (TrkB) signaling axis. Preclinical studies demonstrate that maternal stress during gestation alters the activity of offspring monoaminergic neurons and associated neuroplasticity pathways. Prenatal stress typically reduces serotonergic neuronal firing while enhancing catecholaminergic transmission, whereas pregestational stress may produce opposite neurophysiological effects. These changes are accompanied by behavioral alterations, including increased anxiety- and depression-like behavior. Clinical studies indicate that maternal stress and depression are associated with structural and functional brain alterations in offspring, particularly within the amygdala-hippocampal network involved in emotional regulation. Prenatal antidepressant exposure may modify these outcomes, with effects varying according to drug class, timing of exposure, and maternal clinical status. Although some studies report mild perinatal effects such as earlier delivery or lower birth weight, many associations between prenatal antidepressant exposure and neurodevelopmental disorders appear to be largely explained by underlying maternal psychiatric conditions. The available evidence highlights the complex interaction between maternal mental health, neurotrophic signalling, and monoaminergic neurophysiology in offspring brain development.","PeriodicalId":12514,"journal":{"name":"General physiology and biophysics","volume":" ","pages":"321-334"},"PeriodicalIF":1.5,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147987239","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Polystyrene microplastics size as a key localization determinant for isolated adult cardiomyocytes. 聚苯乙烯微塑料的大小是分离的成人心肌细胞定位的关键决定因素。

IF 1.5 4区生物学

General physiology and biophysics Pub Date : 2026-07-01 DOI: 10.4149/gpb_2026015

Alzbeta Marcek Chorvatova, Michal Cagalinec, Ljuba Bacharova, Dusan Chorvat

引用次数: 0

Quercetin inhibits breast cancer progression by inducing ferroptosis via the NEDD4L-SLC7A11 axis. 槲皮素通过NEDD4L-SLC7A11轴诱导铁下垂抑制乳腺癌进展。

IF 1.5 4区生物学

General physiology and biophysics Pub Date : 2026-07-01 DOI: 10.4149/gpb_2026004

Jiwei Liu, Zhaojun Li, Yanli Ding, Yingyue Zhang, Shuo Shi, Ruonan Meng, Yang Liu, Shujun Liu, Ying Liu, Xiaoying He, Libing Ma, Siyuan Xia, Guojun Liu

{"title":"Quercetin inhibits breast cancer progression by inducing ferroptosis via the NEDD4L-SLC7A11 axis.","authors":"Jiwei Liu, Zhaojun Li, Yanli Ding, Yingyue Zhang, Shuo Shi, Ruonan Meng, Yang Liu, Shujun Liu, Ying Liu, Xiaoying He, Libing Ma, Siyuan Xia, Guojun Liu","doi":"10.4149/gpb_2026004","DOIUrl":"https://doi.org/10.4149/gpb_2026004","url":null,"abstract":"Breast cancer remains one of the most serious malignancies threatening women's health. Quercetin, a major active component found in various Chinese herbal medicines, has shown antitumor potential; however, its specific role and underlying mechanisms in breast cancer require systematic investigation. This study demonstrated through MTT, colony formation, wound healing, and Transwell assays that quercetin significantly inhibits the viability, proliferation, and migration capabilities of breast cancer cells. Transcriptome sequencing combined with biochemical assays, qPCR, and Western blot further indicated that quercetin can induce ferroptosis, which is likely the key mechanism underlying its suppression of malignant progression in breast cancer cells. Mechanistically, by promoting the binding between the E3 ubiquitin ligase NEDD4L and SLC7A11, quercetin induces the ubiquitin-proteasome degradation of SLC7A11, ultimately leading to ferroptosis. Notably, quercetin maintained a significant inhibitory effect even during the malignant transformation of breast cancer cells induced by heavy metal lead (Pb) exposure. Collectively, these findings suggest a potential mechanism by which quercetin may inhibits breast cancer progression through ferroptosis activation via the NEDD4L/SLC7A11 axis, offering preliminary evidence that could support its possible therapeutic application in breast cancer.","PeriodicalId":12514,"journal":{"name":"General physiology and biophysics","volume":"45 4","pages":"335-350"},"PeriodicalIF":1.5,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148712053","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Diagnostic roles and mechanisms of serum IL-33 in liver diseases: A narrative review of recent progress. 血清IL-33在肝脏疾病中的诊断作用及机制：近期进展综述

IF 1.5 4区生物学

General physiology and biophysics Pub Date : 2026-05-01 DOI: 10.4149/gpb_2026001

Mingshuang Wang, Xi Tan

引用次数: 0