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 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 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 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.
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