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Correspondence to Author: Dr. Krathish Bopanna 

Consultant Pharmacologist, Tejhana Consulting LLP, Bangalore, India

DOI: 10.52338/tejoc.2025.5238

Abstract:

Background: The activation of inflammasomes and mitochondrial dysfunction are related mechanisms that contribute to various metabolic, neurodegenerative, and inflammatory diseases. Although curcumin and thymoquinone both possess potent antioxidant and anti-inflammatory properties, their practical use is limited by low bioavailability and an incomplete understanding of their mechanisms. Specifically, the precise biological pathways through which curcumin controls transcription and how thymoquinone protects mitochondria remain poorly understood. The Curcumin–Thymoquinone Complex is a proprietary combination offering new therapeutic options by protecting mitochondria and modulating inflammasome activity across various body systems.
Objective:This review evaluates the experimental evidence demonstrating how CTQ protects mitochondria and inhibits inflammasome activation.
Methods:The author conducted a comprehensive literature search of PubMed, ScienceDirect, and Scopus databases for studies published up to October 2025. Search terms included curcumin, thymoquinone, CTQ, mitochondria, inflammasome, and NLRP3. The evaluation system for preclinical, mechanistic, and translational studies focused on four key outcomes: mitochondrial bioenergetics, oxidative stress, NF-κB/MAPK signalling, and inflammasome activation. The research primarily focused on three areas: in vitro macrophage models for comparison, studies of combined treatments, and animal studies linking mitochondrial measurements to inflammation results. The review was conducted in accordance with the Scope Guidelines and the PRISMA 2020 reporting framework, ensuring a systematically organised, transparent, and reproducible search strategy, eligibility criteria, and evidence synthesis. This integrated methodological approach enhances the scientific credibility and ensures adherence to the scope and translational reliability.
Results:The research showed that CTQ performed better than curcumin alone across all tested macrophage and animal models. It decreased reactive oxygen species, maintained mitochondrial membrane potential, and reduced IL-1β and IL-6 production. These findings indicate that CTQ effectively reduces mitochondrial dysfunction and inflammasome activation, which are essential for treating metabolic, neurodegenerative, and inflammatory diseases, outperforming other compounds. CTQ inhibited NF-κB activation and p38 MAPK phosphorylation, thereby suppressing inflammasome priming, while thymoquinone protected mitochondria from damage, preventing mtROS and mtDNA leakage. CTQ also inhibited caspase-1 activation and cytokine maturation. Furthermore, models studying metabolic and neuroinflammatory processes demonstrated higher mitochondrial enzyme activity, enhanced antioxidant defences, and reduced NLRP3 activation. Pharmacokinetic data reveal that curcumin, when combined in CTQ, exhibits superior solubility, stability, and tissue penetration compared to its use as a standalone agent. Overall, the findings suggest that CTQ functions as an anti-inflammatory agent targeting mitochondria and holds promise for treating metabolic syndrome, NAFLD, ischemic injury, and neurodegenerative diseases.
Conclusion: CTQ combines two phytochemical strategies: curcumin to regulate gene expression and thymoquinone to protect mitochondria. Preclinical evidence indicates that the compound interacts with the inflammasome during both activation and priming stages, producing significant anti-inflammatory and cell-protective effects. Further clinical validation is warranted, but CTQ shows potential as a novel therapeutic approach for diseases caused by mitochondrial dysfunction and inflammasome activation.

Keywords: Curcumin–Thymoquinone Complex (CTQ), Curcumin, thymoquinone, mitochondrial resilience, inflammasome, NLRP3, NF-κB, ROS, translational pharmacology.

Citation:

Dr. Krathish Bopanna, Curcumin–Thymoquinone Complex (CTQ) In Mitochondrial Resilience And Inflammasome Regulation: A Translational Review. The European Journal of Cancer 2026.