We are analyzing https://link.springer.com/article/10.1186/s13098-021-00780-y.

Title:
TLR9 regulates NLRP3 inflammasome activation via the NF-kB signaling pathway in diabetic nephropathy | Diabetology & Metabolic Syndrome
Description:
Background Toll-like receptors (TLRs) are critical sensors for the conservation of bacterial molecules and play a key role in host defense against pathogens. The effect of TLRs on the maintenance of diabetic nephropathy (DN) and resistance to infection has been investigated; however, the detailed effects of TLR9 on DN development remain elusive. Methods We performed quantitative reverse transcription-polymerase chain reaction and western blotting to detect TLR9 expression levels in the kidneys of experimental mice (db/db) and high-glucose-treated mouse mesangial cell strains (MCs). Results TLR9 expression was found to be remarkably upregulated in the kidneys of experimental mice (db/db) and MCs cultivated under hyperglycemic conditions. Moreover, knockdown of TLR9 could restrain NF-kB viability and downregulate the NLRP3 inflammasome in high glucose-treated MCs. TLR9 inhibition also alleviated inflammation and apoptosis, which was reversed by the addition of the NF-κB activator, betulinic acid. Furthermore, depleted TLR9 levels restrained NF-κB viability and NLRP3 expression and reduced kidney inflammation, microalbuminuria discharge, blood sugar level, and glomerular damage in experimental mice (db/db) kidneys. Conclusions These findings offer novel insights into the regulation of TLR9 via the nuclear factor-kB/NOD-, LRR-, and pyrin domain-containing protein 3 inflammasome inflammation pathways in DN progression.
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Keywords {🔍}

tlr, mice, dbdb, expression, article, levels, mcs, pubmed, nlrp, nfkb, diabetic, google, scholar, experimental, inflammasome, knockdown, renal, cas, inflammation, nephropathy, fig, activation, kidney, cell, pathway, protein, data, antibody, abcam, hgtreated, study, level, nuclear, signaling, mesangial, apoptosis, treatment, dbm, strains, found, blood, damage, patients, determine, revealed, role, glomerular, disease, central, nfkbnlrp,

Topics {✒️}

anti-nf-κb/nlrp3 inflammasome-mediated inflammation nf-κb–nlrp3–il-1β pathway negatively tlr9-nf-kb-nlrp3 inflammasome axis nuclear factor-κb inhibitor-α nf-kb-nlrp3 inflammasome pathway nf-kb-nlrp3 inflammasome activation tlr/nf-κb pathway nf-κb pathway activation restrain nf-kb viability high-glucose-stimulated mesangial cells article download pdf c-digit® blot scanner tlr-4/nfκb signalling pathways nf-kb signaling pathway p-nf-κb antibody cold phosphate-buffered saline cysteinyl aspartate-specific proteinase-1 transcription factor nf-kb tlr/myd88/nf-κ ba-treated tlr-knockdown mcs pas-positive mesangial matrix tumor necrosis factor-α semi-quantitative scoring method nf-kb/nlrp3 inflammasomes tumor necrosis factor-alpha experimental tubule-interstitial nephritis nuclear nf-kb levels cardiac-cerebral vascular illnesses analyzed nf-kb activation transcription factor central tlr9-related nlrp3 inflammasome phosphorylated nf-kb levels tlr9-knockdown hg-treated mcs db/db-shrna-tlr9 group p-nf-kb antibody nuclear factor-kb/nod tlr9-regulated nlrp3 inflammasome rho-kinase inhibition prevents administered lentiviral shrna-nc administered lentiviral-shrna-nc nuclear nf-κb tlr9-regulated nf-kb real-time pcr excessive interleukin-1β secretion db/db-shrna-tlr9 mice administered lentiviral-shrna-tlr9 tlr-knockdown experimental mice α-lipoic acid drugs nf-κb activator nlrp3 inflammasome pathways

Schema {🗺️}

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         description:Toll-like receptors (TLRs) are critical sensors for the conservation of bacterial molecules and play a key role in host defense against pathogens. The effect of TLRs on the maintenance of diabetic nephropathy (DN) and resistance to infection has been investigated; however, the detailed effects of TLR9 on DN development remain elusive. We performed quantitative reverse transcription-polymerase chain reaction and western blotting to detect TLR9 expression levels in the kidneys of experimental mice (db/db) and high-glucose-treated mouse mesangial cell strains (MCs). TLR9 expression was found to be remarkably upregulated in the kidneys of experimental mice (db/db) and MCs cultivated under hyperglycemic conditions. Moreover, knockdown of TLR9 could restrain NF-kB viability and downregulate the NLRP3 inflammasome in high glucose-treated MCs. TLR9 inhibition also alleviated inflammation and apoptosis, which was reversed by the addition of the NF-κB activator, betulinic acid. Furthermore, depleted TLR9 levels restrained NF-κB viability and NLRP3 expression and reduced kidney inflammation, microalbuminuria discharge, blood sugar level, and glomerular damage in experimental mice (db/db) kidneys. Conclusions These findings offer novel insights into the regulation of TLR9 via the nuclear factor-kB/NOD-, LRR-, and pyrin domain-containing protein 3 inflammasome inflammation pathways in DN progression.
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            Diabetes
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      headline:TLR9 regulates NLRP3 inflammasome activation via the NF-kB signaling pathway in diabetic nephropathy
      description:Toll-like receptors (TLRs) are critical sensors for the conservation of bacterial molecules and play a key role in host defense against pathogens. The effect of TLRs on the maintenance of diabetic nephropathy (DN) and resistance to infection has been investigated; however, the detailed effects of TLR9 on DN development remain elusive. We performed quantitative reverse transcription-polymerase chain reaction and western blotting to detect TLR9 expression levels in the kidneys of experimental mice (db/db) and high-glucose-treated mouse mesangial cell strains (MCs). TLR9 expression was found to be remarkably upregulated in the kidneys of experimental mice (db/db) and MCs cultivated under hyperglycemic conditions. Moreover, knockdown of TLR9 could restrain NF-kB viability and downregulate the NLRP3 inflammasome in high glucose-treated MCs. TLR9 inhibition also alleviated inflammation and apoptosis, which was reversed by the addition of the NF-κB activator, betulinic acid. Furthermore, depleted TLR9 levels restrained NF-κB viability and NLRP3 expression and reduced kidney inflammation, microalbuminuria discharge, blood sugar level, and glomerular damage in experimental mice (db/db) kidneys. Conclusions These findings offer novel insights into the regulation of TLR9 via the nuclear factor-kB/NOD-, LRR-, and pyrin domain-containing protein 3 inflammasome inflammation pathways in DN progression.
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         Metabolic Diseases
         Endocrinology
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