Bee venom modulates human neutrophil inflammatory functions in Vitro and exerts an anti- inflammatory effect in Vivo in rats.

IF 5.3 2区医学 Q2 IMMUNOLOGY

Inflammopharmacology Pub Date : 2025-06-04 DOI:10.1007/s10787-025-01797-9

Meriem-Dehbia Chabane, Samia Bedouhene, Sahra-Amel Belambri, Nassima Senani, Tinhinane Rekeb, Kahina Ladj, Riadh Ksouri, Pham My-Chan Dang, Jamel El-Benna

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引用次数: 0

Abstract

Bee venom (BV) is a complex bioactive mixture known for its paradoxical ability to exert both pro-inflammatory and anti-inflammatory effects, making it a compelling modulator of inflammatory responses. In this study, we investigated the effect of BV on human neutrophil inflammatory functions in vitro and its effect on inflammation in vivo in rats. Results revealed that BV exhibited a dose-dependent inhibitory effect on formyl-Met-Leu-Phe (fMLF)-induced superoxide production by neutrophils, without affecting PMA-induced superoxide production or superoxide production by the xanthine-xanthine oxidase system. BV was not toxic to neutrophils and did not affect neutrophil adhesion, however, and surprisingly it induced myeloperoxidase release from neutrophils. Interestingly, in vivo BV effectively suppressed xylene-induced ear edema and significantly reduced carrageenan-induced peritonitis by limiting neutrophil recruitment to the peritoneum. These findings suggest that although bee venom can either inhibit or stimulate neutrophil functions in vitro, it still exerts an anti-inflammatory effect in vivo. This dual action highlights the complexity of BV's bioactive components and the importance of targeted therapeutic modulation in inflammatory conditions.

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蜂毒在体外调节人中性粒细胞炎症功能，在体内对大鼠具有抗炎作用。

蜂毒（BV）是一种复杂的生物活性混合物，以其具有促炎和抗炎作用的矛盾能力而闻名，使其成为炎症反应的令人信服的调节剂。在本研究中，我们研究了BV对体外人中性粒细胞炎症功能的影响及其对大鼠体内炎症的影响。结果表明，BV对fMLF诱导的中性粒细胞产生超氧化物具有剂量依赖性的抑制作用，而不影响pma诱导的超氧化物产生或黄嘌呤-黄嘌呤氧化酶系统产生超氧化物。BV对中性粒细胞没有毒性，不影响中性粒细胞粘附，但令人惊讶的是，它诱导中性粒细胞释放髓过氧化物酶。有趣的是，体内BV通过限制中性粒细胞向腹膜的募集，有效抑制二甲苯诱导的耳部水肿，并显著减少卡拉胶诱导的腹膜炎。这些发现表明，尽管蜂毒在体外可以抑制或刺激中性粒细胞的功能，但在体内仍具有抗炎作用。这种双重作用突出了BV生物活性成分的复杂性和炎症条件下靶向治疗调节的重要性。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Inflammopharmacology IMMUNOLOGYTOXICOLOGY-TOXICOLOGY

CiteScore

8.00

自引率

3.40%

发文量

200

期刊介绍： Inflammopharmacology is the official publication of the Gastrointestinal Section of the International Union of Basic and Clinical Pharmacology (IUPHAR) and the Hungarian Experimental and Clinical Pharmacology Society (HECPS). Inflammopharmacology publishes papers on all aspects of inflammation and its pharmacological control emphasizing comparisons of (a) different inflammatory states, and (b) the actions, therapeutic efficacy and safety of drugs employed in the treatment of inflammatory conditions. The comparative aspects of the types of inflammatory conditions include gastrointestinal disease (e.g. ulcerative colitis, Crohn''s disease), parasitic diseases, toxicological manifestations of the effects of drugs and environmental agents, arthritic conditions, and inflammatory effects of injury or aging on skeletal muscle. The journal has seven main interest areas: -Drug-Disease Interactions - Conditional Pharmacology - i.e. where the condition (disease or stress state) influences the therapeutic response and side (adverse) effects from anti-inflammatory drugs. Mechanisms of drug-disease and drug disease interactions and the role of different stress states -Rheumatology - particular emphasis on methods of measurement of clinical response effects of new agents, adverse effects from anti-rheumatic drugs -Gastroenterology - with particular emphasis on animal and human models, mechanisms of mucosal inflammation and ulceration and effects of novel and established anti-ulcer, anti-inflammatory agents, or antiparasitic agents -Neuro-Inflammation and Pain - model systems, pharmacology of new analgesic agents and mechanisms of neuro-inflammation and pain -Novel drugs, natural products and nutraceuticals - and their effects on inflammatory processes, especially where there are indications of novel modes action compared with conventional drugs e.g. NSAIDs -Muscle-immune interactions during inflammation [...]