Tissue & cell最新文献

{"title":"The bioactive compound of traditional herbal ointment accelerates wound closure, epithelialization, and angiogenesis in patients with second-degree burn wound: A randomized clinical trial.","authors":"Mahdi Heydari, Hajir Mehrbani, Seyyed Mohsen Seyyedkazemi, Auob Rustamzadeh, Mohammad Taghi Joghataei, Nader Sadigh, Enam Alhagh Charkhat Gorgich, Hamidreza Alizadeh-Otaghvar","doi":"10.1016/j.tice.2025.102787","DOIUrl":"10.1016/j.tice.2025.102787","url":null,"abstract":"<p><strong>Introduction: </strong>This study endeavors to draw a comparative analysis between a traditional herbal ointment, specifically Swalin, and silver sulfadiazine ointment in the context of repairing deep second-degree burns.</p><p><strong>Methods: </strong>A randomized clinical trial was conducted at the Iran University of Medical Sciences. In this investigation, a cohort comprising eighty-two patients was stratified into two groups, namely Swalin (n = 41) and Silver sulfadiazine (SSD) (n = 41). Over 28 days, ointment applications were administered twice daily. The quantification of ointment compounds was conducted employing Gas Chromatography-Mass Spectrometry (GC-MS). The study encompassed a comprehensive assessment involving clinical examination, quantitative and qualitative histopathological evaluations, pain level determination, and scrutiny of wound closure. Statistical analyses, encompassing chi-square and Mann-Whitney U tests, were performed using SPSS software.</p><p><strong>Results: </strong>Our investigation revealed that the predominant compounds in the ointment were linoleic acid (41.37 %) and elaidic acid (37.45 %). On the 28th day, the Swalin group demonstrated a significantly higher rate of wound closure (81.52 ± 7.76) compared to the SSD group (69.91 ± 2.48) (p < 0.001). Furthermore, a statistically significant distinction was observed between the two groups concerning the degree of epithelialization (P = 0.048). Fibroblast density exhibited a notable discrepancy between the groups (P = 0.02). In terms of angiogenesis and collagen deposition, the Swalin group displayed a significant contrast with the SSD group (P = 0.008 and P = 0.007, respectively), while no statistical distinction was discerned in the number of immune cells (P > 0.05). Histological examination of SSD illustrated a pronounced infiltration of inflammatory cells in the dermis, predominantly lymphocytes. Conversely, the Swalin group exhibited well-formed dermal layers, minimal infiltration, and a profusion of vessels.</p><p><strong>Conclusion: </strong>In conclusion, the findings of this study highlight the potential therapeutic benefits of Swalin ointment, attributed to its rich composition of fatty acids, particularly linoleic acid, and the presence of vitamins C and E.</p>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"93 ","pages":"102787"},"PeriodicalIF":2.7,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143400118","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}

{"title":"Fish and bovine collagen promote higher migration and adhesion of dermal cells pre-treated with wound-healing herbal extracts.","authors":"Marwa Rejeb, Aida Lahmar, Mohamed Bayrem Ghedira, Arem Selmi, Tahsine Kosksi, Nawres Debbabi, Leila Chekir Ghedira","doi":"10.1016/j.tice.2025.102762","DOIUrl":"10.1016/j.tice.2025.102762","url":null,"abstract":"<p><strong>Purpose: </strong>Dermal cells fabricate and interact with the extracellular matrix to preserve structural integrity and further healthy function during wound healing. Collagen is a critical component of the matrix, challenging collagen's stability during wound injury. Natural sources especially plant extracts can promote wound healing and interact with collagen to increase its action. In this context, we studied the effect of extracted fish and bovine collagen in controlling cell proliferation, migration, and adhesion in dermal cells pretreated with plant extract.</p><p><strong>Methods: </strong>An acid-solubilization procedure was used to extract collagen fish (CF) and bovine (CB). Three different hydro-ethanolic extracts were prepared Pistacia lentiscus leaves (PL), Calendula officinalis leaves (FL), and flowers (FS). Migration potency was determined using scratch assay. The covered surface area was estimated after 16 hours and 24 hours after cell seeding. The chemotaxis was determined by the Boyden chamber, and the film was coated with CF or CB (10 µg/mL). or poly-L-lysine (50 µg/mL).</p><p><strong>Findings: </strong>We show that CF and CB increase adherence and migration of 3T3-L1 cells, which are pretreated with PL, FL, and FS. In addition, we highlighted a significantly higher cell adhesion on the CF matrix compared to CB. However, in the case of cells pre-treated with PL, the attachment to CF and CB increased significantly compared to untreated cells. The exposition of Hacat cells to plant extracts regulates the secretion of MMP2 and MMP and the production of reactive oxygen species.</p><p><strong>Conclusion: </strong>CF and CB promote higher migration and adhesion of dermal cells pre-treated with wound-healing herbal extracts. In future studies, composite dressings based on collagen, P. lentiscus, and C. officinalis extracts can potentially be developed for tissue regeneration.</p>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"93 ","pages":"102762"},"PeriodicalIF":2.7,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143371221","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}

{"title":"Application of mRNA technology in neuronal protection of human mature brain-derived neurotrophic factor.","authors":"Liang Wang, Fengjuan Su, Heng Huang, Qiuhong Jiang, Haifang Kong, Zhong Pei","doi":"10.1016/j.tice.2025.102788","DOIUrl":"10.1016/j.tice.2025.102788","url":null,"abstract":"<p><strong>Background: </strong>Although human mature brain-derived neurotrophic factor (hmBDNF) offers potential neuronal protection, its clinical translation remains challenging. Messenger RNA (mRNA) technology is promising in selectively upregulating protein cleavage products. This proof-of-concept study aims to evaluate the neuronal protective effects of hmBDNF mRNA in vitro.</p><p><strong>Methods: </strong>We optimized and synthesized hmBDNF mRNA and conducted dose-response and time-response analyses in SH-SY5Y cells. mRNA expression was assessed via qPCR, while protein expression was evaluated through immunostaining and ELISA. Cell survival rate was measured using cell counting kit-8. We examined cell survival rates in both differentiated and non-differentiated SH-SY5Y cells exposed to H2O2 or serum deprivation following hmBDNF mRNA incubation. Additionally, we assessed the expression of synapse-relevant genes (MAP2, synaptophysin) and the mBDNF receptor (TrkB) in both cell types.</p><p><strong>Results: </strong>The optimized hmBDNF mRNA effectively upregulated hmBDNF expression in SH-SY5Y cells with minimal impact on endogenous proBDNF expression. Dose-response and time-response analyses identified the optimal dose and time point for maximum hmBDNF expression. hmBDNF mRNA significantly increased cell survival in differentiated SH-SY5Y cells expressing MAP2, synaptophysin and TrkB after exposure to oxidative stress or serum deprivation. However, hmBDNF mRNA did not enhance cell survival in non-differentiated SH-SY5Y cells.</p><p><strong>Conclusion: </strong>The optimized hmBDNF mRNA demonstrated a capacity for neuronal protection in vitro. Further in-vivo studies are required to assess its potential for clinical translation.</p>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"93 ","pages":"102788"},"PeriodicalIF":2.7,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143400074","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}

{"title":"Neutrophil extracellular traps-mediated upregulation of HIF-1α promotes corneal neovascularization","authors":"Chunlian Huang ,&nbsp;Dan Zheng ,&nbsp;Jianhai Bai ,&nbsp;Jing Wen ,&nbsp;Xiao Shen","doi":"10.1016/j.tice.2025.102891","DOIUrl":"10.1016/j.tice.2025.102891","url":null,"abstract":"<div><h3>Objectives</h3><div>The objective of this study is to examine the impact of neutrophil extracellular traps (NETs) on angiogenesis, both <em>in vitro</em> and <em>in vivo</em> contexts, as well as to elucidate the regulatory function of hypoxia-inducible factor (HIF-1α).</div></div><div><h3>Methods</h3><div>The study focused on investigating the regulatory function of HIF-1α in the induction of NETs formation. <em>In vivo</em>, following NaOH stimulation, the formation of NETs was quantitatively assessed through immunofluorescence staining employing specific markers, namely SYTOX Green and PicoGreen. Furthermore, mice were administered with HIF-1α, and seven days post-alkali burn, the formation of NETs in the cornea was evaluated by immunofluorescence staining techniques. Protein immunoblotting analysis validated an increase inHIF-1α expression within human umbilical vein endothelial cells (HUVECs) that were induced to form by NETs. <em>In vitro</em>, human neutrophils were subjected to HIF-1α treatment. Subsequent to NaOH stimulation, the NETs mesh was isolated and co-cultured with HUVECs. The migratory capacity and angiogenic potential of HUVECs were then quantitatively evaluated.</div></div><div><h3>Results</h3><div>Upon exposure to NaOH, a notable increase in SYTOX fluorescence was observed in neutrophils, indicative of the formation of a prominent network structure. Furthermore, a marked elevation in HIF-1α protein expression was detected in mouse corneal tissue that had undergone NETs formation, hinting at a potential role of NETs in mediating the up-regulation of HIF-1α. The outcomes of hematoxylin and eosin (H&amp;E) staining, coupled with immunofluorescence staining, revealed an augmentation in neutrophils counts, with NETs exhibiting a marked potentiation of corneal neovascularization. <em>In vitro</em> assessments further demonstrated that HIF-1α played a stimulatory role in promoting the migration and tubular morphogenesis of HUVECs.</div></div><div><h3>Conclusion</h3><div>Exposure to sodium hydroxide serves as a trigger for the induction of NETs formation. NETs mediated an up-regulation of HIF-1α, which subsequently promotes angiogenesis and inflammatory activation in HUVECs. Consequently, this process leads to an enhancement of corneal neovascularization and inflammatory response.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"95 ","pages":"Article 102891"},"PeriodicalIF":2.7,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143776555","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}

{"title":"Exosome-derived Uc.339 as a potential biomarker for bone metastasis from pulmonary adenocarcinoma.","authors":"Weiqiang Lai, Jinchang Huang, Xuwang Lai, Yuli Wang","doi":"10.1016/j.tice.2025.102747","DOIUrl":"10.1016/j.tice.2025.102747","url":null,"abstract":"<p><p>This study explored the role of Uc.339, which is a highly expressed genomic sequence in tumor cell-derived exosomes, in mediating bone metastasis from lung adenocarcinoma. By integrating clinical samples, in vitro experiments, and in vivo murine models, we elucidated the molecular mechanisms underlying this process. Clinical blood samples from patients with lung adenocarcinoma revealed elevated Uc.339 expression in exosomes, particularly in those with bone metastasis. In vitro experiments using A549 cell-derived exosomes demonstrated an increase in osteoclast formation, implicating Uc.339 in bone microenvironment modulation. Mechanistically, Uc.339 functions as a decoy for miR-339-3p, disrupting the gene expression balance. In vivo experiments in a murine model confirmed disrupted bone microstructure in the presence of elevated Uc.339, alongside altered expression of key regulators, including SQSTM1, RANKL, nuclear factor kappa B, and miR-339-3p. Our findings underscore the systemic impact of Uc.339 in exosomes, suggesting its potential as both a biomarker and a mediator of bone metastasis. Moreover, the identified molecular alterations provide potential therapeutic targets for managing bone metastasis in patients with lung adenocarcinoma. This study contributes to a deeper understanding of the complex interplay between cancer cells and the bone microenvironment, paving the way for targeted interventions and improved clinical outcomes.</p>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"93 ","pages":"102747"},"PeriodicalIF":2.7,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143256828","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}

{"title":"Corrigendum to \"PDE4B abrogation extenuates angiotensin II-induced endothelial dysfunction related to hypertension through up-regulation of AMPK/Sirt1/Nrf2/ARE signaling\" [Tissue Cell 91 (2024) 102637].","authors":"Yong Chen, Suipeng Li, Xuqing Hou, Yinfeng Jia","doi":"10.1016/j.tice.2025.102738","DOIUrl":"10.1016/j.tice.2025.102738","url":null,"abstract":"","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":" ","pages":"102738"},"PeriodicalIF":2.7,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143012294","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}

{"title":"The role of lactate metabolism in retinoblastoma tumorigenesis and ferroptosis resistance","authors":"Zhihui Zhang,&nbsp;Junjie Tang,&nbsp;Yaoming Liu,&nbsp;Yinghao Wang,&nbsp;Jinmiao Li,&nbsp;Yang Gao,&nbsp;Chao Cheng,&nbsp;Shicai Su,&nbsp;Shuxia Chen,&nbsp;Siming Ai,&nbsp;Ping Zhang,&nbsp;Rong Lu","doi":"10.1016/j.tice.2025.102893","DOIUrl":"10.1016/j.tice.2025.102893","url":null,"abstract":"<div><div>The Warburg effect, a hallmark of cancer, describes the preference of cancer cells for glucose metabolism via aerobic glycolysis, leading to substantial lactate accumulation. However, the role of lactate metabolism in retinoblastoma, the primary intraocular malignancy in children, remains unclear. This study aimed to elucidate the gene expression profiles associated with lactate metabolism in retinoblastoma and their impact on tumorigenesis and ferroptosis resistance. The involvement of metabolic characteristics in retinoblastoma was analyzed by comparing single-cell RNA sequencing transcriptome profiles from normal retina tissues and retinoblastoma tissues from patient samples. The effects of lactate on retinoblastoma cell line viability and its mechanisms were examined both in vitro and in vivo. Single-cell RNA sequencing analysis revealed enhanced glycolysis in retinoblastoma cells and significant differences in lactate metabolism-related gene expression among various retinoblastoma cell types. Retinoblastoma cell lines with moderate lactate levels exhibited increased viability and resistance to ferroptosis induced by ferroptosis inducers. Additionally, lactate promoted the upregulation of monocarboxylate transporter 1 (MCT1), which facilitated lactate transport, in a dose-dependent manner in retinoblastoma cell lines. Knocking down MCT1 reduced both viability and ferroptosis resistance of retinoblastoma cell lines in a lactate-rich environment. In vivo, disrupting lactate transport through MCT1 inhibition suppressed retinoblastoma tumorigenesis and invasion in a mouse xenograft model, and this effect was reversed by the ferroptosis inhibitor liproxstatin-1. These findings highlighted the crucial role of lactate metabolism in retinoblastoma tumorigenesis and resistance to ferroptosis.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"95 ","pages":"Article 102893"},"PeriodicalIF":2.7,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143783949","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}

{"title":"Ghrelin alleviates inflammation and pyroptosis by inhibiting TNF-α /caspase-8/caspase-3/ GSDME signalling pathways in an in vitro model of high glucose induced liver injury.","authors":"Jingwen Gao, Xinrui Wang, Shengying Ye, Yixin Zhang, Yan Qin","doi":"10.1016/j.tice.2024.102672","DOIUrl":"10.1016/j.tice.2024.102672","url":null,"abstract":"<p><p>Diabetic liver injury (DLI) refers to liver injury resulting from prolonged chronic hyperglycemia and represents a significant complication associated with diabetes, The specific pathogenic mechanism of DLI remains incompletely understood. Tumor necrosis factor α (TNF-α) has been demonstrated to play a crucial role in diabetic complications through intricate signalling pathways, including pyroptosis. However, it remains uncertain whether TNF-α mediates pyroptosis in DLI, we initially established an in vitro model of DLI and confirmed the presence of an inflammatory state characterized by TNF-α in DLI. Furthermore, evidence of gasdermin E (GSDME)-mediated pyroptosis and the activation of cysteinyl aspartate specific proteinase (caspase)-8 was observed in AML-12 cell exposed to high glucose concentrations. We subsequently demonstrated that TNF-α can trigger caspase-8 activation, leading to GSDME-mediated cellular pyroptosis. Furthermore, treatment with ghrelin effectively suppressed hepatic cell pyroptosis induced by high glucose concentrations and provided protection against liver injury. Therefore, we propose that the TNF-α/caspase-8/caspase-3/GSDME pathway represents a novel mechanism underlying pyrodeath in DLI cells and to explore the protective role and molecular mechanisms underlying the effects of ghrelin on DLI by this special pathway, These findings may present potential therapeutic implications for the management of DLI.</p>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"93 ","pages":"102672"},"PeriodicalIF":2.7,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142898180","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}

{"title":"NERP-1 modifications in amyotrophic lateral sclerosis.","authors":"B Noli, G Borghero, M M Mascia, Mustafa Hkir, M Puligheddu, C Cocco","doi":"10.1016/j.tice.2025.102780","DOIUrl":"10.1016/j.tice.2025.102780","url":null,"abstract":"<p><p>VGF peptides, such as NERPs (neuroendocrine regulatory peptides 1 and 2), are derived from amino acids 282-306 and 313-350, respectively, of the human proVGF, which is produced in spinal cord motor neurons. Although certain VGF-derived peptides are changed in ALS, less is known about NERPs. Possible modulations of NERPs and additional VGF peptides (NAPP and TPGH) were investigated using specific antibodies through competitive ELISA in the plasma of ALS patients (at both the initial and advanced phases; n = 46 each vs. 46 controls). As additional controls, naïve PD patients were also enrolled (n = 19 vs. 18 controls) while the potential VGF peptide role in oxidative stress was investigated using a motoneuron-like cell line (NSC34) stressed with sodium arsenate (SA). Western blot (WB) and sephadex chromatography (SC) were used to identify the molecular weight (MW) forms recognized by the VGF antibodies. Exclusively NERP-1 immunoreactivity was changed (elevated) in all plasma samples of ALS patients (compared to controls). Therefore, the NERP-1 antibody was the sole antibody used in ELISA with PD samples and NSC-34 cells. No alterations were seen in PD samples (vs. controls) while NERP-1 immunoreactivity decreased within SA-treated cells but increased in their culture medium. The viability test performed by adding NERP-1 to the stressed cells showed no protective effect. Using WB and SC, we revealed NERP-1 antibody reactivity against various MW forms, including those compatible with the NERP-1 peptide and/or proVGF. NERP-1 is suggested as a possible ALS blood biomarker.</p>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"93 ","pages":"102780"},"PeriodicalIF":2.7,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143400081","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}

{"title":"Role of Tau and Amyloid-beta in autophagy gene dysregulation through oxidative stress.","authors":"Mehrnaz Haghi, Raheleh Masoudi, Fatemeh Ataellahi, Reza Yousefi, Seyed Morteza Najibi","doi":"10.1016/j.tice.2025.102765","DOIUrl":"10.1016/j.tice.2025.102765","url":null,"abstract":"<p><strong>Background: </strong>Alzheimer's disease (AD) is a prevalent neurodegenerative disorder characterized by memory impairment and cognitive decline. Our previous research has demonstrated that pathological Tau and Amyloid-beta (Aβ) disrupt autophagy gene expression, independently. Other studies have shown that these pathological aggregates create a vicious cycle with oxidative stress.</p><p><strong>Methods: </strong>In the current research, the effect of Tau and Amyloid-beta was compared on behavioral function, autophagy gene dysfunction, and oxidative stress in the Drosophila model for AD. Thymoquinone (TQ), an antioxidant agent, was then tested to examine if it could ameliorate the adverse effects of Tau and Amyloid-beta. In addition, the impact of TQ on Tau aggregation was investigated in vitro.</p><p><strong>Results: </strong>Our data showed that Tau and Amyloid-beta induced behavioral disability, autophagy gene dysregulation, and oxidative stress. TQ treatment significantly improved conditions in both types of transgenic flies, with a more profound alleviation in Tau transgenic flies, despite tau having a greater impact on autophagy gene dysregulation. Furthermore, TQ prevented the aggregation of Tau in vitro.</p><p><strong>Conclusion: </strong>To sum up, Tau may exert its toxic effect on autophagy and behavioral dysfunctions significantly through oxidative stress while Amyloid-beta may confer its toxicity through multiple pathways, including oxidative stress. Moreover, since TQ ameliorates the adverse effect of tau and amyloid beta, it could be considered a promising approach for treating AD, probably in combination with other medications against Aβ or Tau.</p>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"93 ","pages":"102765"},"PeriodicalIF":2.7,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143383380","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}