傷口癒合是分子秩序井然的協同過程，過程中任一環節調控異常便可能導致傷口癒合不良。傷口癒合不良原因之一為發炎因子TNF-α與IL-1β顯著升高，引起M1型巨噬細胞過度活化，進而誘發MMP-9過度分泌，破壞傷口處的細胞外基質，以至於傷口的重建和癒合被干擾。同時，M1巨噬細胞透過自泌TNF-α與IL-1β自我刺激，保持在促發炎態，形成一發炎正回饋，導致傷口持續發炎延長癒合時間。在糖尿病患者中，傷口癒合困難更為明顯，因高血糖環境使發炎因子濃度居高不下，持續的發炎反應導致傷口癒合被顯著延遲。過去負離子被提出具有促進血液循環、改善氧化壓力的效用；後生元也曾被提出對於皮膚慢性傷口有所幫助，因此，基於上述背景，高表現量的發炎症因子、MMP-9與M1型巨噬細胞的過度活化，是傷口癒合不佳的主因之一，是故，阻斷M1型巨噬細胞引起的發炎回饋循環是改善傷口癒合的關鍵，在其中的負離子與後生元角色值得探究。
本研究旨在探討負離子與後生元對糖尿病傷口癒合的影響，研究採用鏈脲佐菌素（STZ）誘導糖尿病大鼠模型，建立背部全皮層傷口，實驗分作對照組、糖尿病組、傷口治療組和糖尿病傷口治療共四組。經負離子、後生元處理組的傷口癒合速度與未治療組相比皆顯著加快，同時，負離子與後生元終止傷口的持續發炎，並促進使傷口處膠原蛋白增生、肉芽組織形成與再上皮化發生，使組織修復和傷口癒合。
綜上所述，負離子和後生元兩者可以降低氧化壓力、減少發炎反應，甚至可能可以調節M1型巨噬細胞功能，以加速傷口癒合，在改善傷口癒合方面具潛在應用價值，同時提供急性傷口另一新型、有效的治療策略。

Wound healing is a coordinated process that can be disrupted by regulatory abnor-malities, leading to impaired healing. Elevated inflammatory factors such as TNF-α, IL-1β and hyperactivate M1 macrophages, causing excessive secretion of MMP-9, which de-grades the extracellular matrix and disrupts wound reconstruction. M1 macrophages self-stimulate through autocrine of TNF-α and IL-1β, creating a positive feedback loop of inflammation that prolongs healing. In diabetic patients, high blood sugar exacerbates this issue, keeping inflammatory factor levels high and significantly delaying wound healing.
Previous studies suggest that negative ions can promote blood circulation and reduce oxidative stress, while postbiotics may aid in chronic skin wounds. This study investi-gated the effects of negative ions and postbiotics on diabetic wound healing using a streptozotocin (STZ)-induced diabetic rat model with full-thickness back wounds. The experiment includes four groups: control, diabetes, wound treatment, and diabetes wound treatment. Treatment with negative ions and postbiotics significantly accelerated wound healing compared to untreated groups. Additionally, these treatments reduced persistent inflammation, promoted collagen proliferation, granulation tissue formation, and re-epithelialization, facilitating tissue repair and wound healing.
In summary, negative ions and postbiotics can reduce oxidative stress and inflamma-tion, and potentially regulate M1 macrophage function to accelerate wound healing. These findings suggest their potential application in improving wound healing, offering a novel and effective treatment strategy for wound healings.

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