Brilliant Blue G

Peripheral neuropathy (PN) is a common consequence of peripheral nervous system (PNS) disorders, yet its effective treatment remains a significant clinical challenge. Pyroptosis, an inflammatory form of programmed cell death (PCD) triggered by gasdermin A–E (GSDMA‐E), contributes to the pathogenesis of PN and represents a promising therapeutic target. While reviews of pyroptosis in other diseases are extensive, comprehensive reviews focusing on PN are lacking.

We systematically searched PubMed, Scopus, Web of Science, and Google Scholar (1986–2025). Only original studies investigating pyroptosis in PN were included.

This review first consolidates established evidence, highlighting a context‐dependent dual role of pyroptosis in PN. Its detrimental effects in chronic pain involve canonical (caspase‐1/GSDMD) or noncanonical pathways (e.g., caspase‐4/5/11/GSDMD, caspase‐3/GSDME, caspase‐8/GSDMC), often initiated by inflammasomes (e.g., NOD‐like receptor family pyrin domain containing 3 [NLRP3]). Conversely, its beneficial, tumoricidal role is leveraged in neuroblastoma. Preclinically, diverse inhibitors—including NLRP3 inhibitors (e.g., MCC950), caspase‐1 inhibitors (e.g., VX‐765), and P2X7R antagonists (e.g., Brilliant Blue G)—alleviate pain and promote nerve repair, while pyroptosis inducers (e.g., axitinib) combat chemoresistant tumors. We then identify critical knowledge gaps and emerging frontiers. The roles of most gasdermins (GSDMA, GSDMB, GSDMC) in PN are unknown. We explore the emerging concept of PANoptosis (crosstalk among pyroptosis, apoptosis, and necroptosis) as a novel conceptual framework for PNS pathologies, where shared molecular hubs may amplify neuroinflammation. Furthermore, despite promising strategies like combination therapy and drug repurposing, a significant translational gap exists, with no current clinical trials specifically targeting pyroptosis for PN.

Targeting pyroptosis is a novel therapeutic avenue for PN. This review synthesizes current mechanistic understanding, evaluates preclinical therapeutic strategies, and delineates crucial future directions, including elucidating gasdermin diversity, validating PANoptosis, and bridging the translational divide, thereby accelerating their application for patients suffering from PN.

The transformation of local clay material of Cameroonian origin into magnetic zeolite (Fe@Zeo-4A) for the degradation of acid-blue 90 in solution was investigate herein.The insertion of magnetic iron oxide particles into the zeolitic framework of Zeo-4A was achieved via hydrothermal synthesis.FT-IR spectroscopy, XRD and SEM confirmed the transformation of the clay into zeolite while EDX anal. and elemental mappings confirmed the presence of iron in the magnetic zeolite.Fe@Zeo-4A was strongly attracted to an external magnetic field.N₂ adsorption-desorption studies revealed a considerable decrease in sp. surface area and pore volume from the zeolite to the magnetic zeolite, suggesting the occupation of the pores of the zeolite by magnetite.The central composite design of the response surface methodol. was used as optimization approach for four parameters affecting the efficiency of degradation: solution pH, H₂O₂ concentration, initial dye concentration and time of stirring.ANOVA results revealed good correlation between the exptl. and predicted results as well as the suitability of the linear regression model for describing the dye degradation process.An adjusted correlation coefficient of 85.17% was obtained for the dye degradation model.An optimal degradation percentage of 95.2% was obtained exptl. under optimal conditions of 7.6 for pH, 20 mg/L for dye concentration, 15.0 mol/L for [H₂O₂] and 15 min for time, in close agreement with a theor. response of 96.6% predicted by the model.The magnetic zeolite was found to exhibit good stability over a wide pH range and lost only about 18% of its catalytic efficiency after five cycles of degradation experimentsTherefore, the novel magnetic zeolite-based material is an efficient Fenton catalyst for treating dye-contaminated wastewater.