2021
DOI: 10.3389/fphar.2021.759040
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Methyl Gallate Improves Hyperuricemia Nephropathy Mice Through Inhibiting NLRP3 Pathway

Abstract: Hyperuricemia nephropathy (HN) is a form of chronic tubulointerstitial inflammation, caused by the deposition of monosodium urate crystals (MSU) in the distal collecting duct and medullary interstitium, associated with a secondary inflammatory reaction. Numerous published reports indicated that NLRP3 inflammasome pathway play crucial roles in HN symptoms. The present study aims to investigate the protective effects of methyl gallate on HN mice and the underlying mechanisms. An HN model was established by intra… Show more

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Cited by 16 publications
(6 citation statements)
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“…These three metabolites were classified as flavonoids. Methyl gallate has the ability to block the production of ROS and inhibit the production of inflammation in the kidneys of the human body ( Liu et al, 2021a ). Gallic acid derivatives could also be DNA replication inhibitors as some of the green tea extracts ( López-Lázaro et al, 2011 ).…”
Section: Discussionmentioning
confidence: 99%
“…These three metabolites were classified as flavonoids. Methyl gallate has the ability to block the production of ROS and inhibit the production of inflammation in the kidneys of the human body ( Liu et al, 2021a ). Gallic acid derivatives could also be DNA replication inhibitors as some of the green tea extracts ( López-Lázaro et al, 2011 ).…”
Section: Discussionmentioning
confidence: 99%
“…56 However, increasing evidence suggests that even soluble UA is proinflammatory at clinically relevant concentrations in cell culture and can induce inflammation in animal models of kidney disease and metabolic syndrome, 57,58 indicating that PO-induced asymptomatic HUA also results in renal injury. [59][60][61] Therefore, we examined the potential protective effect of GLPP on renal injury in HUA mice. The results showed that GLPP could reduce PO-induced renal histopathological damage.…”
Section: Papermentioning
confidence: 99%
“…However, judging from the SOD, MDA, and TNF-α factors affected by AeDJF and EeDJF, the mechanism of action may be to inhibit the inflammatory response, as well as to exert free radical scavenging and anti-lipid peroxidation effects. It is speculated that the related signaling pathways may include the NLR inflammatory body signaling pathway [ 44 , 45 ], ERK1/2 signaling pathway [ 46 , 47 ], NF-κB signaling pathway [ 48 ], TLR signaling pathway [ 49 , 50 ], MAPK signaling pathway [ 51 , 52 ], PhoA/ROCK [ 53 ], and PI3K/Akt signaling pathway [ 54 , 55 ].…”
Section: Extractsmentioning
confidence: 99%