Atractylodin ameliorates lipopolysaccharide and d-galactosamine-induced acute liver failure via the suppression of inflammation and oxidative stress

Lyu, Zheng; Ji, Xufeng; Chen, Geng; An, Beiying

doi:10.1016/j.intimp.2019.04.005

Cited by 47 publications

(36 citation statements)

References 45 publications

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“…*Control versus LPS + D-GalN; Ψ LPS + D-GalN versus LPS + D-GalN + Rutin (5 mg/kg, 10 mg/kg, and 20 mg/kg); α Control versus Rutin (5 mg/kg, 10 mg/kg, and 20 mg/kg); φ Rutin (5 mg/kg) versus Rutin (10 mg/kg); δ Rutin (5 mg/kg) versus Rutin (20 mg/kg); and Φ Rutin (10 mg/kg) versus Rutin (20 mg/kg) for Tukey's HSD post hoc analysis at p ≤ .05. (Lee, 2012;Lyu et al, 2019) Control versus Rutin (5 mg/kg, 10 mg/kg, and 20 mg/kg); φ Rutin (5 mg/kg) versus Rutin (10 mg/kg); δ Rutin (5 mg/kg) versus Rutin (20 mg/kg); and Φ Rutin (10 mg/kg) versus Rutin (20 mg/kg) for Tukey's HSD post hoc analysis at p ≤ .05. Ru represents rutin reduced glutathione, and CAT activity (Machawal & Kumar, 2014).…”

Section: Discussionmentioning

confidence: 99%

Protective role of rutin against combined exposure to lipopolysaccharide and D‐galactosamine‐induced dysfunctions in liver, kidney, and brain: Hematological, biochemical, and histological evidences

et al. 2021

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In the era of industrial and social advancement, human being remain in the vicinity of a plethora of toxic substances, including drugs, which not only affect one organ at a time but also impose threat to other organ simultaneously. The two hit effect of combined exposure to lipopolysaccharide (LPS) and D-galactosamine (D-GalN) is well established model to study multiorgan damage and dysfunctioning. Combination of LPS and D-GalN induces hepatic injury is similar to clinical viral hepatitis; hence, this model

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Section: Discussionmentioning

confidence: 99%

Protective role of rutin against combined exposure to lipopolysaccharide and D‐galactosamine‐induced dysfunctions in liver, kidney, and brain: Hematological, biochemical, and histological evidences

et al. 2021

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“…The roots of Atractylodes lancea have been historically used as TCM against rheumatic diseases and digestive disorders (Yu et al, 2017) in China. Several studies have attempted to elucidate the antiinflammatory mechanisms of atractylodin; however, its molecular target remains unclear (Tang et al, 2018;Chuang et al, 2019;Jeong et al, 2019;Lyu et al, 2019). Our results show that atractylodin modulates PEA and OEA levels and suppresses cytokines in LPSactivated microglia in a dose-dependent manner through NAAA inhibition.…”

Section: Discussionmentioning

confidence: 64%

Natural Potent NAAA Inhibitor Atractylodin Counteracts LPS-Induced Microglial Activation

Yang

et al. 2020

Front. Pharmacol.

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N-acylethanolamine-hydrolyzing acid amidase (NAAA) is a lysosomal enzyme that inhibits the degradation of palmitoylethanolamide (PEA), an endogenous lipid that induces analgesic, anti-inflammation, and anti-multiple sclerosis through PPARa activation. Only a few potent NAAA inhibitors have been reported to date, which is mainly due to the restricted substrate-binding site of NAAA. Here, we established a high-throughput fluorescence-based assay for NAAA inhibitor screening. Several new classes of NAAA inhibitors were discovered from a small library of natural products. One of these is atractylodin, a polyethylene alkyne compound from the root of Atractylodes lancea (Thunb) DC., which significantly inhibits NAAA activity and has an IC 50 of 2.81 µM. Kinetic analyses and dialysis assays suggested that atractylodin engages in competitive inhibition via reversible reaction to the enzyme. Docking assays revealed that atractylodin occupies the catalytic cavity of NAAA, where the atractylodin furan head group has a hydrophobic-related interaction with the backbone of the Trp181 and Leu152 residues of human NAAA. Further investigation indicated that atractylodin significantly increases PEA and OEA levels and dose-dependently inhibits LPS-induced nitrate, TNF-a, IL-1b, and IL-6 pro-inflammatory cytokine release in BV-2 microglia. Our results show that atractylodin elevates cellular PEA levels and inhibits microglial activation by inhibiting NAAA activity, which in turn could contribute to NAAA functional research.

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“…**p < 0.01, and ***p < 0.001, the H 2 O 2 vs. control group; ### p < 0.001, the monomers vs. H 2 O 2 group. a low-molecular-weight free radical scavenger that had been implicated in oxidative damage [30]. T-AOC had been recognized as a critical index of oxidative defense [31].…”

Section: Discussionmentioning

confidence: 99%

“…SOD converted superoxide radicals into H 2 O 2 , while CAT degraded H 2 O 2 into water and oxygen [ 29 ]. GSH was a low-molecular-weight free radical scavenger that had been implicated in oxidative damage [ 30 ]. T-AOC had been recognized as a critical index of oxidative defense [ 31 ].…”

Section: Discussionmentioning

confidence: 99%

Four active monomers from Moutan Cortex exert inhibitory effects against oxidative stress by activating Nrf2/Keap1 signaling pathway

Zhang

Luo

et al. 2020

Korean J Physiol Pharmacol

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Atractylodin ameliorates lipopolysaccharide and d-galactosamine-induced acute liver failure via the suppression of inflammation and oxidative stress

Cited by 47 publications

References 45 publications

Protective role of rutin against combined exposure to lipopolysaccharide and D‐galactosamine‐induced dysfunctions in liver, kidney, and brain: Hematological, biochemical, and histological evidences

Protective role of rutin against combined exposure to lipopolysaccharide and D‐galactosamine‐induced dysfunctions in liver, kidney, and brain: Hematological, biochemical, and histological evidences

Natural Potent NAAA Inhibitor Atractylodin Counteracts LPS-Induced Microglial Activation

Four active monomers from Moutan Cortex exert inhibitory effects against oxidative stress by activating Nrf2/Keap1 signaling pathway

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