Toll-like receptor 7 involves the injury in acute kidney ischemia/reperfusion of STZ-induced diabetic rats

Abstract

PURPOSE:To determine whether Toll-like receptor 7 (TLR7) is the potential targets of prevention or progression in the renal ischemia/ reperfusion (I/R) injury of STZ-induced diabetic rats. METHODS:Thirty six Sprague-Dawley rats were randomly arranged to the nondiabetic (ND) or diabetic group (DM), with each group further divided into sham (no I/R injury), I/R (ischemia-reperfusion) and CD (given by Chloroquine) group. Preoperatively, Chloroquine (40 mg/kg, intraperitoneal injection.) was administrated 6 days for treatment group. I/R animals were subjected to 25 min of bilateral renal ischemia. Renal function, histology, apoptosis, cytokines, expression of TLR7, MyD88 and NF-κB were detected. RESULTS:The serum levels of blood urea nitrogen, creatinine, IL-6 and TNF-α, apoptotic tubular epithelial cells, expression of TLR7, MyD88 and NF-κB were significantly increased in DM+I/R group, compared with ND+I/R group (p<0.05). All these changes were further improved by TLR7 inhibition Chloroquine except Paller scores (p<0.05). CONCLUSION:Toll-like receptor 7 inhibition attenuates the acute renal ischemia/reperfusion injury of STZ-induced diabetic in SD rats.

Study the Effect of Apocynin on Some Renal Functions in Ischemia / Reperfusion Injury in Male Albino Rats

“…These finding are also supported by those found by Yayi et al [21] who stated that, Apocynin has beneficial effect on renal function and improved the kidney damage which occurred after I/R injury. Furthermore, Munshi et al [22] declared that, Apocynin improved the increased urea and creatinine in I/R may be attributed to depletion of energy rich phosphates (ATP) caused by shortage of oxygen during ischemia, which leads to apoptosis and necrosis of tubular cells.…”

Effect of Paclitaxel+Hirudin on the TLR4-MyD88 Signaling Pathway During Inflammatory Activation of Human Coronary Artery Smooth Muscle Cells and Mechanistic Analysis

“…After binding with endogenous ligands, such as heat shock protein 60, intracellular fibronectin and oxygenized low-density lipoprotein, this molecule can be activated immediately and then transfer activation signals to downstream inflammatory pathways to mediate inflammatory reactions and induce cell proliferation and differentiation [37]. TLR4 can be activated by the exogenous ligand LPS, causing self-dimerization and exerting its functions via MyD88-dependent and independent channels [38,39]. The MyD88-dependent channel binds with interleukin-1 receptorassociated kinase (IRAK) via its death domain to cause self-phosphorylation of IRAK, activate tumor necrosis factor receptor-associated factor 6, activate c-Jun N-terminal protein kinase to induce the latter to activate I-κB α and β kinase, promote the activation of NF-κB and its transfer into the nucleus to initiate transcription, synthesize and secrete downstream inflammatory factors, and ultimately aggravate systemic and local inflammatory reactions.…”

TLR7 in B cells promotes renal inflammation and Gd-IgA1 synthesis in IgA nephropathy

“…Studies involving animal models have shown that TLR7 is involved in the pathogenesis of glomerulonephritis, including lupus nephritis and diabetic nephropathy; agonists of TLR7 aggravate glomerulonephritis symptoms in both diseases, while the blockade of TLR7 could alleviate renal injury (61-64). High renal TLR7 expression has been detected in both lupus-prone mice and a diabetic animal model, and it is closely related to the production of proinflammatory cytokines (e.g., IL-6, IL-1β, TNF-α, and IL-12) and consequent renal injury (61,(63)(64)(65). The infiltration of B cells and increased expression of TLR7 has been demonstrated in kidney specimens of patients with lupus nephritis (25,26,66).…”