Effect of Taoren Honghua Jian Granule on NLRP3 Inflammasome Expression in Patients with Stable Coronary Artery Disease: A Multi-Center, Double-blind, Randomized Controlled Trial

To evaluate the clinical efficacy of Taoren Honghua Jian Granule (THJ) in stable coronary artery disease (SCAD) patients with syndrome of qi stagnation and blood stasis, and to investigate its effect on the expression of NOD-like receptor family pyrin domain containing 3 (NLRP3) inflammasome in peripheral blood mononuclear cells (PBMCs).

In this multicenter, double-blind, randomized controlled trial, 80 eligible SCAD patients from 3 Shanghai hospitals were randomly assigned to receive either the THJ (18.3 g, twice daily, orally) or a matched placebo for 4 weeks 40 in each group, followed by a 4-week follow-up. Chinese medicine (CM) Syndrome Scores and Seattle Angina Questionnaire (SAQ) assessments were conducted pre- and post-intervention. Quantitative PCR was used to analyze mRNA levels of NLRP3 inflammasome components [NLRP3, apoptosis-associated speck-like protein (ASC), caspase-1, interleukin (IL)-1β, and IL-18] in PBMCs, while ELISA was used to detect plasma inflammatory cytokines [IL-10, IL-1β, IL-2, IL-6, IL-8, IL-18, tumor necrosis factor (TNF-α), and high-sensitive C-reactive protein (hs-CRP)].

After 4 weeks of treatment, the overall treatment efficacy was higher in the treatment group than in the placebo group; the CM syndrome scores of the two groups were significantly lower after treatment, and the THJ group was considerably lower than the placebo group (P<0.05, P<0.01). The THJ group had significantly higher scores for 5 SAQ dimensions than the placebo group (P<0.01). Both mRNA expression of NLRP3 inflammasome components (NLRP3, ASC, caspase-1, IL-1β, IL-18) decreased in PBMCs (P<0.01). In addition, plasma levels of IL-2, IL-8, IL-18, and TNF-α significantly decreased in THJ group compared with the placebo group after treatment (P<0.05, P<0.01).

THJ alleviates angina symptoms and improves quality of life in SCAD patients, potentially through NLRP3 inflammasome inhibition and subsequent attenuation of pro-inflammatory cytokine release. These findings position THJ as a promising adjunct therapy for inflammation-driven coronary atherosclerosis. (Registration No. ChiCTR1900021772).