JIN Xiao-min, ZHANG Xiao-xi, GUO Lu, et al. Effect and Mechanism of Total Flavonoids from Smilacis Glabrae Rhizoma in Treatment of Gouty Arthritis Based on NLRP3 Inflammasomes Axis[J]. Chinese journal of experimental traditional medical formulae, 2018, 24(4): 90-95.
JIN Xiao-min, ZHANG Xiao-xi, GUO Lu, et al. Effect and Mechanism of Total Flavonoids from Smilacis Glabrae Rhizoma in Treatment of Gouty Arthritis Based on NLRP3 Inflammasomes Axis[J]. Chinese journal of experimental traditional medical formulae, 2018, 24(4): 90-95. DOI: 10.13422/j.cnki.syfjx.2018040090.
Objective: To observe the anti-inflammatory effect of total flavonoids from Smilacis Glabrae Rhizoma (TFSG) on acute gouty arthritis and its mechanism. Method: Totally 90 C57BL/6 mice were randomly divided into the normal group
the model group
the colchicine group (0.65 mg·kg-1)
and the TFSG group (100
300
500 mg·kg-1)
with 15 mice in each group. The acute gouty arthritis model was induced with monosodium urate (MSU) crystals
except for the normal group
and the mice's ankle swelling degree was measured. The mice's synovium tissues were collected to detect the inflammatory mediators interleukin-1β (IL-1β)
IL-6 and tumor necrosis factor-α (TNF-α) by enzyme-linked immunosorbent assay. The protein expressions of Nod-like receptor protein 3 (NLRP3)
apoptosis-associated speck-like protein (ASC)
and cysteine aspartic acid protease-1 (Caspase-1) were detected by Western blot
and the mRNA expressions of NLRP3
ASC
and Caspase-1 messenger in synovium tissues were detected by Real-time PCR. Result: Compared with the normal group
mice ankle swelling degree of the model group increased significantly (P<0.01)
and the levels of IL-1β
IL-6
TNF-α and the protein and mRNA expressions of NLRP3
ASC and Caspase-1 were significantly increased (P<0.01). Compared with the model group
the TFSG group could significantly reduce ankle swelling degree and IL-1β
IL-6 and TNF-α levels (P<0.01)
as well as NLRP3
ASC
Caspase-1 protein and mRNA expressions(P<0.01). Conclusion: TFSG has an anti-gouty arthritis effect
and its mechanism is correlated with NLRP3 inflammasome axis.