Andrographis paniculata constituent-mediated anti-inflammatory and immune modulation pathways

The entry "Anti-inflammatory effect via Andrographis paniculata constituents/immune modulation/heat-clearing action" does not refer to a single canonical therapeutic target, but rather describes the broad pharmacological actions attributed to multiple bioactive compounds found within the medicinal plant *Andrographis paniculata*. The primary active molecule is andrographolide—a diterpene lactone—alongside related analogs such as neoandrographolide. These compounds exert their effects by modulating several key inflammatory signaling pathways: most notably inhibiting NF-kB activation and downstream proinflammatory cytokines like TNF-alpha and IL-6; suppressing MAPK/iNOS activity; regulating chemokine gene expression; and influencing TLR/MyD88-dependent immune responses. Traditionally classified as a “cold” herb in Chinese medicine for its heat-clearing properties, *A. paniculata* is widely used for treating infections, inflammation-related conditions such as sepsis, respiratory tract infections, autoimmune diseases, and even cancer adjunctively. However, because this entry refers collectively to plant extracts’ mechanisms rather than an individual receptor/enzyme/transporter/protein target recognized by modern pharmacology nomenclature systems—it should be flagged as not a true therapeutic target but rather an herbal mechanism profile.

Other names

Andrographis paniculata extractAndrographolide (major active constituent)Neoandrographolide, dehydroxyandrographolide (other key constituents)Herba AndrographisSambiloto (traditional name)

The anti-inflammatory and immunomodulatory effects are mediated by: Inhibition of NF-kB pathway activation, reducing transcription of pro-inflammatory genes such as TNF-alpha and IL-6; Downregulation of iNOS expression and NO production via p38MAPK pathway suppression; Modulation of chemokine gene expression including ENA-78, RANTES, MCP-1 in inflamed tissues/cells; Suppression of TLR/MyD88/NF-kB signaling axis in immune cells leading to reduced cytokine storm responses during infection or sepsis models.