Pranindya Sari Astari, Susanto Agus Dwi, Indarto Dono
Doctoral Program of Medical Sciences, Faculty of Medicine, Universitas Sebelas Maret, Jalan Ir. Sutami No. 36A, Surakarta, 57126, Indonesia.
Department of Pulmonology and Respiratory Medicine, Faculty of Medicine, Universitas Sebelas Maret, Surakarta, Indonesia.
Inflammopharmacology. 2025 Apr 17. doi: 10.1007/s10787-025-01745-7.
Pyroptosis, a highly inflammatory form of programmed cell death, plays a key role in diseases such as sepsis, rheumatoid arthritis, Alzheimer's disease, and COPD. It is driven by inflammasome activation, leading to the release of pro-inflammatory cytokines. Pyridoxine (Vitamin B6), an essential micronutrient with known anti-inflammatory effects, has been suggested as a potential regulator of inflammasome activation and pyroptosis. This review examines current evidence on pyridoxine's role in modulating pyroptosis.
A literature search was conducted in PubMed, Scopus, and Web of Science for studies published between 2014 and 2024. The search focused on pyridoxine's relationship with inflammation, inflammasomes, and pyroptosis pathways using keywords such as "pyridoxine," "Vitamin B6," "pyroptosis," "inflammasome," "caspase-1," and "gasdermin D." Both preclinical and human studies were reviewed, with emphasis on molecular mechanisms underlying pyridoxine's anti-inflammatory effects.
Studies consistently showed that pyridoxine reduced inflammasome activation, decreased pro-inflammatory cytokine production, and inhibited caspase-1 (CASP-1) activity, thereby suppressing pyroptosis. Human studies, though indirect, linked higher pyridoxine levels to reduced systemic inflammation, suggesting a possible anti-pyroptotic effect.
Pyridoxine shows potential as an anti-pyroptotic agent due to its anti-inflammatory and immunomodulatory properties. However, further well-designed clinical trials are needed to confirm its role in controlling pyroptosis, especially in diseases associated with excessive inflammasome activation.
细胞焦亡是一种高度炎症性的程序性细胞死亡形式，在脓毒症、类风湿性关节炎、阿尔茨海默病和慢性阻塞性肺疾病等疾病中起关键作用。它由炎性小体激活驱动，导致促炎细胞因子的释放。吡哆醇（维生素B6）是一种具有已知抗炎作用的必需微量营养素，已被认为是炎性小体激活和细胞焦亡的潜在调节剂。本综述研究了关于吡哆醇在调节细胞焦亡中作用的现有证据。
在PubMed、Scopus和Web of Science中检索2014年至2024年发表的研究。检索重点是吡哆醇与炎症、炎性小体和细胞焦亡途径的关系，使用了“吡哆醇”、“维生素B6”、“细胞焦亡”、“炎性小体”、“半胱天冬酶-1”和“gasdermin D”等关键词。对临床前和人体研究均进行了综述，重点关注吡哆醇抗炎作用的分子机制。
研究一致表明，吡哆醇可降低炎性小体激活，减少促炎细胞因子产生，并抑制半胱天冬酶-1（CASP-1）活性，从而抑制细胞焦亡。人体研究虽然间接，但将较高的吡哆醇水平与全身炎症减轻联系起来，提示可能具有抗细胞焦亡作用。
由于其抗炎和免疫调节特性，吡哆醇显示出作为抗细胞焦亡剂的潜力。然而，需要进一步设计良好的临床试验来证实其在控制细胞焦亡中的作用，特别是在与炎性小体过度激活相关的疾病中。
