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关键词： 网状内皮组织增生病   Viperin蛋白   相互作用   结构域   IFN  

摘要： 网状内皮组织增殖病病毒（REV）是一种重要的家禽免疫抑制性病原，干扰素诱导内质网关联病毒抑制蛋白（Viperin）是一种由干扰素诱导产生的宿主抗病毒蛋白，目前REV复制与Viperin之间的关系尚不清楚。本试验首先将REV接种DF-1，通过荧光定量PCR（RT-qPCR）探究REV感染对宿主Viperin表达的影响。随后，构建鸡Viperin真核表达质粒，分别通过基因过表达和siRNA干扰技术检测Viperin对REV复制的影响。为探究Viperin影响REV复制的机理，构建了Viperin N、SAM和C结构域的真核表达质粒，并通过RT-qPCR和Western blot检测转染上述质粒对REV复制的影响。最后，通过RT-qPCR检测了Viperin表达与IFN信号通路的关系。结果显示，REV感染上调DF-1中Viperin的转录水平。过表达Viperin在感染早期（12 h-24 h）抑制REV的复制，而在感染后期（36 h-72 h）促进REV复制；Viperin特异性siRNA试验结果与过表达试验结果一致。将pEGFP-Viperin-N、pEGFP-Viperin-SAM、pEGFP-Viperin-C质粒分别转染DF-1细胞，感染后期（36 h-72 h）Viperin的N结构域和SAM结构域抑制REV复制，而Viperin的C结构域促进REV复制。IFN信号通路相关分子的检测结果表明，过表达Viperin后，IFN-α的表达水平在24 h和72 h呈现下调趋势，IFN-β在12-48 h呈现下调趋势，IFN-γ在36-72 h呈现下调趋势。综上所述，REV感染促进Viperin的转录，而Viperin的过表达在REV感染后期可能通过调控IFN信号通路促进REV的复制，其C端结构域是发挥调控作用的关键结构域。本研究揭示了REV感染和宿主Viperin蛋白的相互作用关系，为深入阐明鸡Vieprin调控病毒复制的机制提供了科学数据。

摘要： In the original publication [...].

关键词： 针指震颤行气法   艾灸   神阙穴  

摘要： 探讨针指震颤行气法联合艾灸对慢性盆腔炎患者TNF-α/IL-10平衡及盆腔微循环的影响。方法 纳入222.05-2024.10蒲江县中医医院收治的240例慢性盆腔炎患者为研究对象,按分层随机法分为三组,各80例,A组进行艾灸神阙穴治疗,B组进行针指震颤行气法治疗,C组进行针指震颤行气法联合艾灸神阙穴治疗,对比三组组治疗方法的效果。结果 C组患者的治疗总有效率高于A组、B组(P<0.05)。治疗前三组中医证候评分对比,未见统计差异(P>0.05),治疗后C组分值明显比A组、B组少(P<0.05)。治疗前三组TNF-α/IL-10比值对比,未见统计差异(P>0.05),治疗后C组比值明低于A组、B组(P<0.05)。治疗前三组的子宫动脉RI、PI及盆腔血流量未见对比差异(P>0.05),治疗后C组的子宫动脉RI、PI低于A组、B组,C组的盆腔血流量高于A组、B组(P<0.05)。结论 针指震颤行气法联合艾灸神阙穴治疗应用效果良好,能够促进TNF-α/IL-10平衡,改善盆腔微循环,促进康复可推广使用。

关键词： Galectin-3   NF-κB   TLR4   microglia   neuron apoptosis  

摘要： OBJECTIVES:High blood levels of galectin-3 (Gal-3) predict poor outcomes after intracerebral hemorrhage (ICH). Our previous study also showed that Gal-3 could aggravate ICH-induced brain injury through increasing neuroinflammatory activation and nerve cell death. In this study, we focus on the role of Gal-3 in nerve cell death after ICH. METHODS:An ICH mice model and an co-stimulation model were established to study Gal-3's effect on neuron cell death via toll-like receptor 4 (TLR4)/nuclear factor kappa-B (NF-κB) pathway. Western blot and immunofluorescence (IF) staining were applied for neuron apoptosis evaluation. Enzyme-linked immunosorbent assay (ELISA) was used to measure the production of neuroinflammation factors. RESULTS:Gal-3 expression in microglia was increased and positively correlated with the severity of neurological impairment after ICH. Terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) and NeuN (or MAP2) double staining assay results revealed that the increasing of neuron cell apoptosis after Gal-3 treatment both in and co-stimulation experiments could be reversed by treatment with Gal-3 inhibitor MCP, TLR4 inhibitor TAK-242, NF-κB inhibitor PDTC, or TNF-α inhibitor C87 effectively. ELISA results revealed the same trends of TNF-α release changes from microglia after Gal-3 or inhibitor treatment both and . WB results confirmed the Gal-3's role on apoptosis by the expression level of proteins such as FADD, Apaf-1, Bax, Cytochrome C, Caspase-8, and cleaved-Caspase-3 in neuron cells. CONCLUSION:The upregulation of Gal-3 in microglia after ICH could aggravate neuron cell apoptosis through increasing TNF-α release via TLR4/NF-κB pathway.

关键词： Cervical Cancer   Head and Neck Cancer   Immunosuppression   Immunotherapy   T cell  

摘要： BACKGROUND:Human papillomavirus type 16 (HPV16) positive cancers have a tumor environment that induces antigen-presenting cells to increase IL-23 expression. Unclear is if HPV16 E6/E7 oncoproteins expressed in these cancers play a role in upregulating interleukin (IL)-23 in the tumor microenvironment (TME), and how this cytokine impacts the antitumor cytotoxic T-cell response in HPV16+ cancer. METHODS:CD8 T-cells targeting HPV16+ cancer cells were isolated from C57BL/6 mice bearing HPV16+ C3.43 tumors that were therapeutically vaccinated against HPV16 E6/E7 and incubated with IL-23. These T-cells were then co-incubated with HPV16+ target cells in a cytotoxicity assay to assess their cytolytic capacity. Additionally, carboxyfluorescein succinimidyl ester (CFSE) labeled T-cells were used to track the effect of IL-23 on their proliferation. The effect of IL-23 neutralization on vaccine-induced antitumor immunity during tumor progression was studied in vivo to assess its potential as either a standalone treatment or combined with a vaccine targeting HPV16 E6/E7. HPV16- tumors were engineered to express E6/E7 to find out if these oncoproteins upregulate IL-23. To understand how HPV oncoproteins in the TME affect transcriptional regulation of IL-23 producing cells, we used single-cell Assay for Transposase-Accessible Chromatin (ATAC)+RNA sequencing. RESULTS:Inside macrophages residing in the HPV+ TME, transcription factor enrichment and linkage analysis identified KLF2 as a potential regulator of Il23a. Overexpression of KLF2 in macrophages upregulates IL-23 production. CD8 T-cells that recognize HPV16+ cells incubated with IL-23 are inhibited in both their killing and proliferative capacities. IL-23 neutralization increased the presence of HPV-specific cytotoxic CD8 T-cells inside the HPV16+TME in an IL-17 independent manner. Combination of IL-23 neutralization followed by HPV16 E6/E7 vaccination increases survival by amplifying the anti-tumor immune response. CONCLUSION

关键词： 厄贝沙坦片   苯磺酸氨氯地平片   难治性高血压   疗效   TNF-α  

摘要： 评价厄贝沙坦片(IRB)联合苯磺酸氨氯地平片(AMB)对于难治性高血压(RH)的治疗有效性。方法 选择70例RH患者,随机数字表均分,实验组选择IRB联合AMB治疗;对照1组选择IRB单一治疗;对照2组选择AMB单一治疗,对比三组的总有效率、血压水平、肿瘤坏死因子-α(TNF-α)水平、动脉粥样硬化指标。结果 实验组的总有效率高于对照1组、对照2组;实验组治疗后的血压水平、TNF-α水平均低于对照1组、对照2组;实验组治疗后的动脉粥样硬化指标优于对照1组、对照2组(P<0.05)。结论 IRB联合AMB能够提高RH患者的总有效率,稳定患者的血压水平,且能减轻炎症反应,预防动脉粥样硬化,具有较高的联合用药优势。

关键词： 系统性血管炎   补体C3   疾病活动度   补体C4   炎症标志物  

摘要： 探讨血清补体C3、C4水平检测在系统性血管炎活动期判断中的临床应用价值。方法 选取2023年7月至2024年8月于我院诊治的80例系统性血管炎患者,根据疾病活动程度评分将患者分为活动期组(45例)和缓解期组(35例)。结果 活动期组患者血清C3、C4水平低于缓解期组,而ESR、CRP、VEGF等炎症指标高于缓解期组(P<0.05)。ROC曲线分析显示,血清C3、C4联合检测对系统性血管炎活动期的诊断效能优于单一指标。多因素Logistic回归分析表明,血清C3、C4水平下降是系统性血管炎活动期的独立危险因素(P<0.005)。结论 血清补体C3、C4水平检测对系统性血管炎活动期判断具有重要的临床价值,可作为疾病活动度评估的重要参考指标,有助于临床医师对系统性血管炎的诊断、治疗方案制定及预后评估。

关键词： Apical periodontitis   Rheumatoid arthritis   Endodontic infection   Inflammatory process   Bone resorption   Endodontics  

摘要： This study aimed to evaluate the influence of rheumatoid arthritis on the inflammatory and resorptive process of periapical lesions in an animal model. Forty Wistar rats were divided into four groups (n = 10): control (C), apical periodontitis (AP), rheumatoid arthritis (RA), and AP + RA. RA was induced by two injections into the caudal subcutaneous tissue containing 50 mu L volume of methylated bovine albumin (Met-BSA, 40 mg/mL) and 5% glucose emulsified with CFA/complete Freund's adjuvant (Mycobacterium sp), and a third intra-articular injection in the right knee with half of the same solution. The right knee width was measured throughout the experimental period. AP was induced by pulp exposure of the right upper and lower first and second molars. After 30 days, the animals were euthanized, and the joints were processed for descriptive analysis using hematoxylin-eosin (H&E) staining. The hemi-mandibles were also removed and the inflammatory infiltrate was analyzed by H&E and immunohistochemistry for IL-6, IL-17, TNF-alpha, and the resorptive process by RANKL, OPG, TRAP, and micro-CT analysis. Statistical tests were applied (p < 0.05). The periapical lesions of the AP + RA group exhibited a more intense inflammatory infiltrate and a more exacerbated immune profile for IL-17 and TNF-alpha compared to the AP group (p < 0.05). Micro-CT analysis revealed larger lesions in the AP + RA group and greater immunostaining for RANKL and TRAP compared to the AP group (p < 0.05). It can be concluded that RA exacerbates periapical inflammation and bone resorption of AP, increasing the levels of IL-17, TNF-alpha, TRAP, and RANKL.

关键词： HaCaT keratinocyte cells   Protocatechuic acid derivatives   Anti-inflammatory effect   Skin care cosmetics  

摘要： BackgroundThe skin plays a vital role in host defense against microorganisms, viruses, and environmental agents. Inflammatory skin conditions are initiated by increased expression of cytokines, interferons, and interleukins, which activate immune responses. TNF-alpha and lipopolysaccharide (LPS) are key inducers of skin inflammation, contributing to diseases, including psoriasis, ichthyosis, atopic dermatitis, and potentially melanoma. Protocatechuic acid (PCA), a natural anthocyanin with anticancer and anti-inflammatory properties, was chemically modified to synthesize PCA alkyl ester (PAE) derivatives to improve its anti-inflammatory *** study aimed to investigate whether PAE derivatives more effectively inhibit TNF-alpha-induced inflammation in HaCaT keratinocyte cells compared to unmodified PCA. The expression levels of key downstream molecules in the Akt signaling pathway were assessed by western blotting, and the relative mRNA expression of muscle atrophy-related genes was analyzed using real-time *** evaluated cytokine expression using ELISA, and MTT assays were performed to assess cytotoxicity. The PAE derivatives, particularly PAE-5, 6, and 7, significantly reduced IL-8 production at lower concentrations than PCA while maintaining low cytotoxicity. In contrast, PAE-12 exhibited reduced efficacy despite higher hydrophobicity, suggesting that excessive hydrophobicity may hinder biological activity. Moreover, PAE-5 and PAE-6 markedly suppressed LPS-induced expression of IL-6, IL-1 beta, and TNF-alpha, underscoring the importance of optimal alkyl chain *** results provides that PCA alkyl ester derivatives are promising anti-inflammatory agents with low toxicity, offering potential applications in cosmeceutical formulations for treating inflammatory skin conditions.