“…Sinapic acid prevented STZ-induced DKD in rats by attenuating inflammation and OS through upregulating Nrf2/HO-1 signaling pathways [132]. Calycosin ameliorated kidney injury and dysfunction in HFD-fed/STZ-induced diabetic rats by inhibiting inflammation, and OS through modulating the IL33/ST2, NF-κB, and Nrf2 signaling pathways [114]. ↓FN, ↓vimentin, ↓α-SMA, ↑ E-cadherin, ↑ZO-1, ↓MMP9, ↓ROS, ↑Nrf2 [152] AGEs, advanced glycation end products; AngII, angiotensin II; α-SMA, α-smooth muscle actin; AT1/2R, angiotensin II receptor type 1/2; CAT, catalase; CIN, contrast induced nephropathy; CKD, chronic kidney disease; COX2, cyclooxygenase 2; CRAD, chronic renal allograft dysfunction; DHE, dihydroethidium; DKD, diabetic kidney disease; EMT, epithelial-to-mesenchymal transition; eNOS, endothelial nitric oxide synthase; FSGS, focal segmental glomerulosclerosis; γ-GCS, γ-glutamine cysteine synthase; GPx, glutathione peroxidase; GR, glutathione reductase; GSK3β, glycogen synthase kinase 3β; GST, Glutathione-S-transferase; HFD, high fat diet; HG, high glucose; HIF, hypoxia-inducible factor; HMGB1, high-mobility group box 1; HO-1, Heme oxygenase-1; iNOS, inducible nitric oxide synthase; LDH, lactate dehydrogenase; LN, lupus nephritis; LPS, lipopolysaccharide; MCP-1, monocyte chemoattractant protein-1; MDA, malondialdehyde; MDCK, Madin-Darby canine kidney; MMP, matrix metalloproteinase; NLRP3, NLR family pyrin domain containing 3; Nqo1, NADPH quinone oxidoreductase; Nrf2, nuclear factor erythroid 2-related factor 2; OS, oxidative stress; ox-LDL, oxidized low-density lipoprotein; RAS, renin-angiotensin system; SOD, superoxide dismutase; STZ, Streptozotocin; UUO, unilateral ureteral obstruction.…”