Objective:　To　study　the　therapeutic　effects　of　Shenyuan　Gan　(参远苷,　SYG)　on　the　inflammatory　response　in　BV2　microglial　cells　induced　by　lipopolysaccharide　(LPS).　Methods:　The　cytotoxicity　of　SYG　to　BV2　microglial　cells　was　evaluated　using　a　Cell　Counting　Kit-8　(CCK-8)　assay,　and　the　effect　of　SYG　concentrations　on　LPS-induced　BV2　microglial　cells　was　studied.　The　morphological　changes　were　observed　using　an　optical　microscope.　The　nitric　oxide　(NO)　concentration　in　cell　culture　supernatant　was　determined　using　Griess　reagent.　The　expression　of　cytokines　and　inflammatory　mediators　were　also　measured　by　an　enzyme-linked　immunosorbent　assay　(ELISA).　Western　blot　analysis　was　used　to　determine　the　levels　of　inducible　NO　synthase　(iNOS),　nuclear　factor-kappa　B　(NF-κB)　p65,　alpha　inhibitor　of　NF-κB　(IκB-α),　phosphorylation-IκB-α　(p-IκB-α),　NOD-like　receptor　3　(NLRP3),　and　caspase-1　expression.　Moreover,　the　expression　of　iNOS,　NLRP3,　and　ionized　calcium　binding　adapter　molecule　1　(Iba1)　was　also　observed　using　immunofluorescent　staining.　Results:　SYG　had　a　low　cytotoxic　effect　on　BV2　microglial　cells　and　could　significantly　decr-ease　LPS-induced　morphological　changes　of　BV2　microglial　cells　(P　＜　0.05).　ELISA　results　showed　that　SYG　significantly　inhibited　the　LPS-induced　increase　in　interleukin　(IL)-1β　and　IL-6　in　BV2　microglia　cells　(P　＜　0.05),　and　Western　blot　analysis　showed　that　the　phosphorylation　levels　of　iNOS,　NF-κB　p65,　and　IκB-α　as　well　as　NLRP3　and　caspase-1　expression　were　also　significantly　decreased,　and　IκB-α　expression　was　increased　after　SYG　treatment　(P　＜　0.05,　compared　with　the　LPS-treated　group).　The　immunofluorescence　results　were　consistent　with　the　Western　blot　results,　and　Iba1　staining　indicated　that　the　cell　morphology　tended　to　be　resting.　These　results　indicate　that　SYG　has　a　certain　inhibitory　effect　on　LPS-induced　inflammation　in　BV2　microglial　cells.　Conclusion:　SYG　can　inhibit　LPS-induced　release　of　inflammatory　factors　in　BV2　microglial　cells　by　affecting　the　phosphorylation　levels　of　NF-κB　p65　and　IκB-α.　SYG　is　a　valuable　candidate　for　treating　neuroinflammation-related　diseases.　©　2022　Digital　Chinese　Medicine