Neuroinflammation constitutes the primary pathological mechanism underlying neurodegeneration, with chronic neuroinflammatory responses driving detrimental secondary damage to neural tissues. Polygonum multiflorum is a traditional Eastern medicinal herb historically utilized as a hematopoietic agent and applied in the management of diverse pathological conditions. The objective of this study was to evaluate and compare the anti-inflammatory efficacy of standard, commercially available P. multiflorum (C1) against a KIOM-patented, in vitro-propagated variant of P. multiflorum (K1). The K1 variant possesses elevated biomass and a higher concentration of active constituents, and both variants were evaluated under culture and cultivation conditions of lipopolysaccharide (LPS)-induced neuroinflammation. Following LPS stimulation and subsequent treatment with either C1 or K1 in murine microglial BV-2 cells, we evaluated nitric oxide (NO) generation, the secretion of pro-inflammatory cytokines, inducible NO synthase (iNOS) expression, mitogen-activated protein kinase (MAPK) phosphorylation, and transcription factor activity. Additionally, antioxidative capacity was measured via DPPH radical scavenging assays alongside NO production metrics. Both C1 and K1 successfully suppressed the expression of iNOS and cyclooxygenase-2 (COX-2), while also reducing the secretion of pro-inflammatory cytokines. To elucidate the underlying regulatory pathways, Western blotting was employed to quantify inflammatory mediators, including interleukin (IL)-1β, IL-6, tumor necrosis factor (TNF)-α, MAPKs, and IκBα. Furthermore, C1 and K1 attenuated the activation of both p38 and nuclear factor-kappa B (NF-κB) within the LPS-stimulated BV-2 microglia. Across all experimental parameters, K1 demonstrated superior anti-neuroinflammatory efficacy at a lower dosage compared to C1, a property attributed to its enhanced biomass content. Consequently, K1 displays greater therapeutic potential than C1 and holds promise for broader application in the development of preventative and therapeutic interventions for various inflammation-driven neurodegenerative disorders.
