Fig 1: Proposed mechanistic model depicting the inhibitory effects of baicalein on lipopolysaccharide (LPS)-induced inflammasome activation in H9c2 cardiomyoblasts. Baicalein exerts multilevel suppression of the LPS-triggered inflammatory cascade in H9c2 cardiomyoblasts. Following LPS exposure, canonical TLR4 signaling activates NF-κB, leading to transcriptional priming of NLRP3, Casp1, and Il1b. Mitochondrial stress and elevated ROS further promote NLRP3 inflammasome assembly, resulting in caspase-1 activation and proteolytic maturation of IL-1β and IL-18, culminating in inflammatory cytokine release and cytotoxic injury. Baicalein, administered prior to LPS challenge, inhibits both the priming arm (NF-κB activation and NLRP3 induction) and the activation arm (mitochondrial dysfunction, ROS overproduction, and caspase-1 activity), thereby limiting downstream IL-1β/IL-18 maturation and reducing inflammation-associated cytotoxicity. The schematic summarizes the integrated points of interference experimentally demonstrated across Figure 1 - 4.