Histology and histopathology, Vol.41, Nº4, (2026)
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- PublicationOpen AccessDaphnetin alleviates renal inflammation, oxidative stress, and apoptosis in septic rats via the JAK2/STAT3 signaling pathway(2026) Pan Hu; Qingye Li; Yinglin Wang; Ruliang Yao; Zhuo Zhang; Biología Celular e Histología; Universidad de Murcia, Departamento de Biología Celular e HistologíaAcute kidney injury (AKI) induced by sepsis is a critical condition with high morbidity, posing a significant challenge in clinical settings. Daphnetin (DAP), a natural compound, has demonstrated anti inflammatory and antioxidant properties in various diseases. This study aims to explore the specific role and underlying mechanism of DAP in sepsis-induced AKI. Sepsis was induced in rats using the cecal ligation and puncture (CLP) method. Renal tissue samples were analyzed via hematoxylin and eosin staining for histopathological analysis and TUNEL assay for apoptosis detection. The expression of proteins associated with apoptosis or the JAK2/STAT3 pathway was determined via western blot analysis. Inflammatory cytokines were measured using ELISA kits. Oxidative stress markers were detected via biochemical analysis. Additionally, an in vitro sepsis model induced by lipopolysaccharide (LPS) was established to validate the effects of DAP. Cytotoxicity of DAP to HK-2 cells was determined using the CCK-8 assay, and cell apoptosis was analyzed via flow cytometry analysis. The results showed that DAP remarkably improved renal function in septic rats; it reduced the levels of inflammatory cytokines (TNF-α, IL-1β, IL-6), attenuated oxidative stress, and suppressed cell apoptosis in renal tissues. DAP inhibited the activation of JAK2/STAT3 signaling in both septic rats and LPS-stimulated HK-2 cells. In vitro experiments showed that DAP or AG490 (a JAK2 inhibitor) alleviated LPS-induced apoptosis, inflammation, and oxidative stress. In conclusion, DAP attenuates sepsis-induced AKI by reducing inflammation, oxidative stress, and apoptosis via the inactivation of the JAK2/STAT3 pathway.
- PublicationOpen AccessComparable expression of stem markers and damage-responsive proteins in untreated and chemoradiation-treated rectal cancer(2026) Sachi Sekine; Hirotoshi Kawata; Tomoko Kamiakito; Takeo Nakaya; Yasuyuki Miyakura; Koichi Suzuki; Toshiki Rikiyama; Akira Tanaka1; Kentaro Tsuji; Biología Celular e Histología; Universidad de Murcia, Departamento de Biología Celular e HistologíaPurpose. Cancer stem cells (CSCs) are suggested to contribute to therapy resistance in rectal cancer. However, histopathological analysis of CSCs is still lacking in rectal cancer. Methods. The expression of leucine-rich, repeat containing G protein-coupled receptor 5 (LGR5), proto oncogene, polycomb ring finger 1 (BMI1), yes associated transcriptional regulator (YAP) and its paralog TAZ (hereafter, YAP/TAZ), and nuclear β catenin was compared in untreated and chemoradiation treated (CRT) rectal cancer by in situ hybridization and immunostaining. Niche factors were also compared in human rectal cancer specimens and the embryonic intestine. Results. The mean ratios were 15% and 14% for LGR5, 30% and 33% for BMI1, 2.7% and 7.6% for YAP/TAZ, and 38% and 32% for nuclear β-catenin in untreated and CRT rectal cancer, respectively, showing no significant differences for these stem markers following CRT. The stromal expression ratios of YAP/TAZ were 9.7% and 23% in untreated and CRT rectal cancer, which indicated significant upregulation and confirmation of the damage response in the stroma of CRT tumors. In addition, cancer cells co-expressing LGR5 and CDKN1B are also comparable in untreated and CRT rectal cancer. For niche factors, we found that WNT2B and GREM1 were uniformly expressed in rectal cancer with a pattern similar to that of the early embryonic intestine. Conclusion. The expression of LGR5, BMI1, CDKN1B, and YAP/TAZ was comparable in untreated and CRT rectal cancer. The uniform expression of mesenchymal niche factors might prevent the zonation of the stem cell niche in rectal cancer
- PublicationOpen AccessTumor promotion or suppression: Revisiting the role of EXT1 and heparan sulfate(2026) Hiroyuki Tomita; Akira Hara; Ayumi Niwa; Biología Celular e Histología; Universidad de Murcia, Departamento de Biología Celular e HistologíaHeparan sulfate (HS), a linear sulfated polysaccharide attached to proteoglycans, modulates the availability and activity of growth factors and cytokines to regulate cell signaling, adhesion, and migration. Exostosin-1 (EXT1), a key glycosyl-transferase for HS chain elongation, is increasingly implicated in cancer development and progression. Although originally identified as a tumor suppressor in hereditary multiple exostoses, EXT1 exhibits a complex, context-dependent role in cancer. The effects of EXT1 in cancer differ by cell and tumor type, exerting both tumor-suppressing and tumor-promoting effects. Notably, EXT1 also alters the tumor microenvironment via its expression in stromal fibroblasts and endothelial cells, further influencing tumor behavior. This review discusses the functions of HS and EXT1, emphasizing the roles of EXT1 in cancer and its microenvironment. A deeper understanding of these mechanisms may offer novel therapies targeting the HS biosynthetic pathway.
- PublicationOpen AccessTreatment strategies for locally advanced and metastatic urothelial carcinoma based on molecular profiles: A Review(2026) Ken Fukiage; Takafumi Minami; Marco Antonio De Velasco; Kazutoshi Fujita; Mamoru Hashimoto; Biología Celular e Histología; Universidad de Murcia, Departamento de Biología Celular e HistologíaUrothelial carcinoma (UC), which includes bladder carcinoma (accounting for 90-95% of cases) and upper urinary tract carcinoma (comprising 5-10%), is one of the most prevalent malignancies worldwide. For several decades, platinum-based chemotherapy has been the primary treatment modality for this disease. However, recent advancements have significantly transformed the therapeutic landscape for patients with UC. This transformation has been facilitated by the introduction of various treatment options, including immune checkpoint inhibitors targeting PD-L1 or PD-1, antibody-drug conjugates that target nectin-4 or trophoblast cell surface antigen 2 expressed on cancer cells, and fibroblast growth factor receptor (FGFR) inhibitors specifically indicated for Patients with UC with FGFR3 mutations. Although these novel therapies have demonstrated marked survival benefits for patients with locally advanced or metastatic UC, their efficacy can vary depending on the specific molecular profile present on cancer cells. In this review, we summarize the molecular classifications of UC and the corresponding treatment landscape associated with these classifications.
- PublicationOpen AccessLong non-coding RNA C20orf56 as a predictor of response to neoadjuvant CCRT and survival rates of rectal cancers(2026) Cheng-Fa Yeh; Ching-Chieh Yang; Yi-Kai Kao; Pin-Chun Chen; Po-Wen Yang; Sung-Wei Lee; Yu-Feng Tian; Yu-Hsuan Kuo; Li-Ching Wu; Chien-Feng Li; Yi-Che Chang Chien; I-Wei Chang; Chih-I Chen; Biología Celular e Histología; Universidad de Murcia, Departamento de Biología Celular e HistologíaIntroduction. Colorectal cancer is the third most prevalent malignancy and the second leading cause of cancer mortality worldwide. Neoadjuvant concurrent chemoradiotherapy (CCRT) improves survival and increases curative surgery rates in rectal cancer. C20orf56, a long non-coding RNA (lncRNA), plays diverse roles in cancer, but its association with neoadjuvant CCRT response and prognosis in rectal cancer remains unexplored. Materials and Methods. Tumor samples from 343 rectal cancer patients who received neoadjuvant CCRT followed by surgery were analyzed for C20orf56 expression via in situ hybridization. Associations between C20orf56 expression and clinicopathological parameters were evaluated with the χ² test. Survival outcomes were assessed using the Kaplan-Meier method and compared by log-rank tests, while multivariate analysis was conducted using a Cox proportional hazards model. Additionally, an independent cohort of responders and non-responders (n=8 per group) was used to validate C20orf56 transcript levels by real-time RT-PCR. Results. A transcriptomic analysis (GSE35452) identified C20orf56 as differentially expressed between responders and non-responders. Decreased expression of C20orf56 showed significant correlations with less advanced post-treatment tumor invasiveness, negative post-treatment nodal metastasis, absence of vascular invasion and perineural invasion, and improved response to neoadjuvant CCRT (all p≤0.024). Diminished expression of C20orf56 was associated not only with favorable disease-specific survival (DSS), local recurrence-free survival (LRFS), and metastasis-free survival (MeFS) (all p<0.0001) in univariate analysis but also functioned as an independent predictor signifying enhanced clinical outcomes, including DSS, LRFS, and MeFS (all p<0.001). In the real-time RT-PCR analysis, the transcriptomic levels were significantly lower in the responder group compared with the non-responder group (p=0.007). Conclusion. C20orf56 may play a significant role in rectal cancer progression and response to neoadjuvant CCRT, serving as a novel prognostic factor.
- PublicationOpen AccessPenning decoction ameliorated pyroptosis in mice with lipopolysaccharide-induced endometritis through inhibition of the TLR4/NF-κB/NLRP3 pathway(2026) Chen Chen; Yuqiong Yuan; Zhihui Liu; Qianru Zhou; Jiani Shi; Biología Celular e Histología; Universidad de Murcia, Departamento de Biología Celular e HistologíaObjectives. Endometritis, stemming from bacterial infection, manifests as persistent inflammation and may cause infertility. Penning decoction (PND) has been approved for clinical treatment of patients with endometritis. However, the mechanism by which it prevents endometritis remains unknown. This study aimed to examine the impact of PND on lipopoly saccharide (LPS)-induced endometritis and elucidate the underlying mechanisms involved. Methods. Firstly, ultra-performance liquid chromatography-quadrupole-time-of-flight mass spectrometry (UPLC-Q-TOF-MS) analysis, in which both positive and negative ion modes were used to identify the chemical compounds in PND, was performed. The antipyroptotic effects of PND were validated in LPS-induced endometritis mice. Additionally, mouse endometrial epithelial cells (MEECs) were used to explore the molecular mechanism of PND in serum in vitro. Results. A total of 145 chemical compounds, including flavones, saponins, polysaccharides, alkaloids, and glycosides, were identified in positive and negative ion modes. The results showed that LPS could induce pyroptosis in endometritis in vivo and in vitro. Treatment with PND or serum containing PND could significantly ameliorate LPS-induced pyroptosis by inhibiting the activation of the TLR4/NF-κB/NLRP3 signaling pathway. Conclusion. Our results demonstrated that PND may improve LPS-induced endometritis by inhibiting the TLR4/NF-κB/NLRP3 pathway, which provides a potentially effective drug for the clinical treatment of endometritis.
- PublicationOpen AccessRadix Actinidiae chinensis inhibits neovascularization in colorectal cancer and its mechanism(2026) Minyuan Chen; Jiante Li; Jieyu Liu; Ziqi Meng; Biología Celular e Histología; Universidad de Murcia, Departamento de Biología Celular e HistologíaObjective. Colorectal cancer is one of the most common cancers worldwide, and its angiogenesis is a key factor in tumor growth and metastasis. Radix Actinidiae chinensis is considered to have antitumor activity in traditional Chinese medicine, but its effect on neovascularization in colorectal cancer has not been clarified. Herein, we aimed to evaluate the effect of different concentrations of Radix Actinidiae chinensis on the neovascularization of colorectal cancer and explore its possible mechanisms. Method. A mouse model of colorectal cancer was established, and mice were randomly divided into control, low-, and high-concentration groups. Then the mice in the experimental group were treated with Radix Actinidiae chinensis, and its effects on neovascularization and tumor growth were evaluated by tumor growth curve tracking, immunohistochemical analysis, vessel density assessment, RT-qPCR, and protein immunoblotting to explore the underlying mechanisms. Results. It was shown that tumor tissues in the high concentration group exhibited significantly slower growth in both mass and volume compared with the low concentration and control groups. Immunohistochemical staining revealed a reduction in the expression of the vascular endothelial marker CD31 in the Radix Actinidiae chinensis treatment group. Moreover, the protein expression levels of vascular markers in tumor tissues showed a slight decrease in the low-concentration group and a marked reduction in the high-concentration group. These findings suggest that angiogenesis in the tumor microenvironment was inhibited in a concentration-dependent manner, with protein expression levels closely mirroring gene expression patterns. Conclusion. The study found that Radix Actinidiae chinensis inhibits neovascularization in a dose dependent manner in a mouse model of colorectal cancer. These results provide experimental support for its potential use as a therapeutic agent against colorectal cancer, suggesting that it may suppress tumor growth and metastasis by inhibiting angiogenesis.
- PublicationOpen AccessBrazilin attenuates kidney ischemia- reperfusion injury by regulating inflammation, oxidative stress, and mitochondrial dysfunction(2026) Lulu Zhang; Fei Mu; Ying Yu; Chen Cui; Meng Tang; Kexin Sun; Yanping Yin; Jingwen Wang; Rui Gong; Jinyi Zhao; Biología Celular e Histología; Universidad de Murcia, Departamento de Biología Celular e HistologíaBrazilin, a natural homoisoflavonoid, is the primary bioactive ingredient derived from the bark and heartwood of Caesalpinia sappan L. It has been proven to exhibit multiple biological activities and therapeutic potential in chronic degenerative diseases, fibrotic disorders, inflammatory diseases, and cancers. However, whether it is involved in regulating the pathological process of acute kidney injury (AKI) is not fully understood. This study aimed to elucidate the role and key pharmacological molecular mechanisms of brazilin in AKI. Our data demonstrated that pretreatment with brazilin can significantly reduce the high expression of serum creatinine (Scr), blood urea nitrogen (BUN), and lipocalin-2 (LCN2) in mice exposed to ischemia/ reperfusion (I/R) and alleviate kidney histopathological damage. Meanwhile, pretreatment with brazilin can alleviate apoptosis, inflammation, and oxidative stress injury in the kidney tissue cells by partially inhibiting the Toll-like receptor 4 (TLR4)/nuclear factor-kappa B (NF-κB)/NOD-like receptor family pyrin domain containing 3 (NLRP3) inflammatory pathway or activating the nuclear factor erythroid 2-related factor 2 (Nrf2)/heme oxygenase‐1 (HO-1) antioxidant pathway. In vitro, pretreatment with brazilin significantly downregulated pro-apoptotic Bax and upregulated anti apoptotic Bcl-2 expression in human renal proximal tubular cells (HK-2) subjected to oxygen-glucose deprivation/reoxygenation (OGD/R). Besides, it ameliorated mitochondrial dysfunction by enhancing mitochondrial biogenesis and restoring mitochondrial membrane potential. These effects collectively suppressed oxidative stress injury and NLRP3 inflammasome signaling pathway activation. In summary, brazilin exhibits significant protective effects against I/R-induced AKI by attenuating inflammation, oxidative stress and cell apoptosis, and mitochondrial damage. These findings suggest that brazilin holds promise as a potential therapeutic agent for AKI.
- PublicationOpen AccessAlteration in epithelium and stroma of post-INTACS cornea: Ultrastructure and 3D transmission electron tomography(2026) Omar Kirat2; Adrian Smedowski; Aljohara Alkanaan; Fahad Almoqbel; Turki Almubrad; Saeed Akhtar; Biología Celular e Histología; Universidad de Murcia, Departamento de Biologia Celular e HistiologiaThis study was conducted to investigate the ultrastructure of the epithelium and stroma of post INTACS corneas. INTACS were surgically inserted into the corneas of three patients to remodel the keratoconus shape. INTACS were inserted with the IntraLase femtosecond laser. Patients 1, 2, and 3 returned to the clinic 8, 6, and 9 years, respectively, after surgery due to their deteriorating vision. The lamellae above the INTACS were removed surgically and processed for light and electron microscopy. 2D and 3D digital images of lamellae, collagen fibrils (CFs), and proteoglycans (PGs) were captured by a bottom-mounted camera and analysed using iTEM software. The epithelium and stromal lamellae had degenerated. A large number of aggregates of microfilaments were present in the Bowman’s layer (BW) and throughout the stroma. In the stroma, just above the INTACS insertion, lamellae were completely disorganised and running randomly in the large electron-lucent spaces. The CF diameter was significantly smaller than in the normal cornea. 3D images showed microfibrils within the CF were less in the post-INTACS cornea than in the normal cornea. We believe that insertion of the INTACS disturbed the lamellar organisation and uniform distribution of CFs. This non-uniform CF distribution increased over time, resulting in vision impairment.
- PublicationOpen AccessMicroscopic studies on the structure of microornamentation and adhesive setae in normal and regenerating tail scales of some geckos(2026) Lorenzo Alibardi; Antonio Bonfitto; Biología Celular e Histología; Universidad de Murcia, Departamento de Biologia Celular e HistiologiaThe present review summarizes recent information on the formation and fine structure of epidermal microornamentation and adhesive setae in scale pads of the tail in some arboreal geckos. The study utilizes transmission and scanning electron microscopy, in conjunction with immunolabeling, to detect the main proteins of the microornamentation, known as Corneous Beta Proteins. These are special small proteins with a central region containing beta-sheets that form most of the corneous material of scales and pads. These proteins are packed into long cords that form short spinulae or longer setae. In tail scales, the spinulae feature different shapes but possess a limited size, 0.5-2.0 µm. In sparse areas located toward the distal part of the tail, some scales form adhesive pads, and their microornamentation grows longer, forming setae of 10-30 µm in length in the species studied herein. This process gives rise to stiff but flexible bristles that arboreal geckos use for adhesion on vertical or inverted substrates or tree branches. During tail regeneration, some scales also regenerate the adhesive setae and give rise to new adhesive pads. Caudal setae are formed by a process similar to that observed during the formation of digital setae. This derives from the interaction of a specific epidermal layer (clear) with another layer (Oberhäutchen), which are formed in the scale pads. Setae vary in length, diameter, or terminal arborization, and they resemble those of the digits, albeit shorter. The presence of caudal adhesive pads reinforces the prehensibility and maneuverability of these arboreal lizards in their environment.
- PublicationOpen AccessLactylation formation, gene regulation, biological functions, and clinical relevance(2026) Zhimei Qiu; Youyang Huang; Qing Guo; Ying Li; Yongchao Zhao; Bei Shi; Xiaoyu Wei; Biología Celular e Histología; Universidad de Murcia, Departamento de Biologia Celular e HistiologiaLactate, as an end-product of glycolysis, has been considered as a metabolic waste that participates in a few physiological functions. Recently, a novel study by Zhao’s laboratory reported that lactate can serve as an epigenetic modification substrate, causing histone or nonhistone lysine residues to undergo lactylation, which then regulates gene transcription, translation, and protein function. Subsequent studies confirmed that lactylation plays an important role in a series of physiological and pathological processes, such as inflammation, cancer, and other biological processes. In this review, we summarize advanced achievements on the effects of lactylation in various diseases and potential treatment targets, providing a reference and direction for future research.
- PublicationOpen AccessEarly i-IFTA: Associated factors and impact on graft outcome(2026) Tristan De Nattes; Damien Sizaret; Philippe Gatault; Christine Bonenfant; Claire Kizlik; Lucie Maigret; Marie-Christine Machet; Marion Rabant; Juliette Gueguen; Elodie Miquelestorena-Standley; Antoine Taillandier; Biología Celular e Histología; Universidad de Murcia, Departamento de Biología Celular e HistologíaAssessment of inflammation in scarred cortical parenchyma of kidney transplant (i-IFTA) is a criterion for chronic active T cell-mediated rejection (TCMR) and has mainly been explored in one-year protocol biopsies. We evaluated the factors, molecular profile, and one-year graft outcome associated with early i-IFTA. We included 101 kidney transplant biopsies performed within the first six months posttransplant (median=89 days), between 2009 and 2020. Interstitial inflammation Banff criteria were retrospectively re evaluated, and diagnosis reclassification was performed according to the Banff 2022 classification. After re evaluation, 85% of the biopsies presented no rejection, including 16% of biopsies from patients with delayed graft function, and 5% of biopsies with BK polyoma virus nephropathy. Eleven per cent (11%) of the biopsies presented histological TCMR. Delayed graft function was associated with i-IFTA severity (OR=2.78, 95% CI:1.01-7.68, p=0.049). The molecular profile obtained in 93 biopsies revealed that 86% presented a no-rejection profile and that a TCMR molecular profile tended to be more frequent in biopsies with i-IFTA2/3 compared with i-IFTA0/1 (17% vs. 4%, p=0.060). I-IFTA0/1 and 2/3 presented comparable one-year graft outcomes, including donor-specific antibodies (DSA), rejection occurrence, and graft function. In conclusion, early i IFTA is an ambiguous and non-specific lesion that can be associated with ischemia/reperfusion injury, early BK nephropathy, or rejection.
- PublicationOpen AccessRHCG inhibition promotes the sensitivity of PIK3CA-mutant non-small lung cancer to PI3K inhibitor(2026) Muqun Wang; Yingying Pang; Haitao Liu; Biología Celular e Histología; Universidad de Murcia, Departamento de Biología Celular e HistologíaPIK3CA, the gene encoding the catalytic subunit of the PI3K complex, is significantly amplified and mutated in several cancer forms, including non small cell lung cancer (NSCLC). Although follicular lymphoma and chronic lymphocytic leukemia have been treated clinically with PI3K inhibitors, there are currently no FDA-approved medications targeting PI3K mutations in lung cancer. In this study, by TCGA database analysis, we found that RHCG was highly expressed in PIK3CA-mutated NSCLC and was associated with poor prognosis. Knockdown of RHCG in PIK3CA-mutated NSCLC inhibited cell proliferation and promoted apoptosis, thereby sensitizing cells to PI3K inhibitors. Mechanistically, the knockdown of RHCG acts synergistically with PI3K inhibitors to produce more effective inhibition of AKT and S6RP phosphorylation downstream of PI3K. This finding suggests a potential NSCLC target with PIK3CA mutations.
- PublicationOpen AccessGuishen-erxian decoction can improve ovarian function in rats with premature ovarian failure by inhibiting oxidative stress and granulosa cell DNA fragmentation mediated by the PI3K/Akt/FOXO3a pathway(2026) Yuhua He; Wenhui Wang; Yingyun Liu; Danna Chen; Yongqi Shen; Chengjie Liang; Huanmei Zhong; Biología Celular e Histología; Universidad de Murcia, Departamento de Biología Celular e HistologíaBackground. The aim of this study was to establish a rat model of premature ovarian failure (POF) with cyclophosphamide (CTX), and explore the molecular basis of POF and the mechanism of Guishen Erxian Decoction (GSEXD) to improve POF from the perspective of oxidative stress regulation of ovarian granulosa cell (OGC) DNA fragmentation. Method. The study utilized SD rats to establish a POF model via CTX. Rats were divided into Control, POF group, three GSEXD dosage groups (low, medium, high), and a GSEXD+PI3K agonist group to assess GSEXD’s therapeutic effects on oxidative stress, DNA fragmentation and ovarian damage. Result. GSEXD can improve the body weight, ovarian index, pathological status, and hormone secretion of POF rats, and inhibit ovarian oxidative stress and DNA fragmentation. In addition, GSEXD inhibits the activation of the PI3K/Akt/FoxO3a pathway. PI3K agonist 740 Y-P can reverse the effects of GSEXD on ovarian function, ovarian antioxidant capacity, and granulosa cell DNA fragmentation in POF rats. Conclusion. Inhibition of oxidative stress damage and excessive DNA fragmentation of granulosa cells is a key pathway for GSEXD to promote follicle growth and development and alleviate ovarian function decline, which may be related to the inhibition of the PI3K/AKT/FOXO3a pathway by GSEXD.
- PublicationOpen AccessCalycosin accelerates wound healing in diabetic rats by alleviating oxidative stress and promoting angiogenesis(2026) Min Lu; Lifen Xue; Mi Zhou; Meifeng Zhang; Huifeng Zhu; Wei Lu; Biología Celular e Histología; Universidad de Murcia, Departamento de Biología Celular e HistologíaBackground. Angiogenesis is a physiological process of diabetic wound healing. Although calycosin has been reported to exert protective effects on diabetic nephropathy, its role and mechanisms in diabetic wound healing remain unclear. This study investigates the effects of calycosin on wound healing and angiogenesis, and the role of the Nrf2/HO-1 pathway in mitigating oxidative stress in diabetic rats. Methods. In vivo, type 2 diabetes (T2DM) in Sprague-Dawley (SD) rats was induced by a high-fat diet for six weeks combined with a single intraperitoneal injection of 45 mg/kg streptozotocin (STZ). The anesthetized diabetic rats underwent a full skin excision on the back and were then treated with calycosin for two weeks to evaluate the protective effect of calycosin on oxidative stress associated with the Nrf2/HO-1 pathway in diabetic wound rats. In vitro, damage to Human Umbilical Vein Vascular Endothelial Cells (HUVECs) was induced by high glucose, and then treated with calycosin or combined with Nrf2 agonist to evaluate whether calycosin affects cell activity and inhibits oxidative damage via the Nrf2/HO-1 pathway. Results. Our results indicate that calycosin promotes angiogenesis by activating the Nrf2/HO-1 signaling pathway and upregulating downstream antioxidant genes, thereby accelerating wound healing. In vitro studies have also shown that Nrf2/HO-1 signaling activation can enhance the promoting effect of calycosin on cell activity and the inhibitory effect on oxidative stress in HUVECs induced by high glucose. Conclusion. Our results show that calycosin can accelerate wound healing by promoting angiogenesis and inhibiting oxidative stress mediated by the Nrf2/HO 1 pathway, which provides a theoretical basis for the treatment of refractory diabetic wounds.