The Effect of Autophagy on Inflammation Cytokines in Renal Ischemia/Reperfusion Injury

Abstract

Acute kidney injury (AKI) is characterized by a rapid loss of kidney function and an antigen-independent inflammatory process that causes tissue damage, which was one of the main manifestations of kidney ischemia/reperfusion (I/R). Recent studies have demonstrated autophagy participated in the pathological process of acute kidney injury. In this study, we discuss how autophagy regulated inflammation response in the kidney I/R. AKI was performed by renal I/R. Autophagy activator rapamycin (Rap) and inhibitor 3-methyladenine (MA) were used to investigate the role of autophagy on kidney function and inflammation response. After the experiment, kidney tissues were obtained for the detection of autophagy-related protein microtubule-associated protein light chain 3(LC3)II, Beclin1, and Rab7 and lysosome-associated membrane protein type (LAMP)2 protein by reverse transcription-polymerase chain reaction (PT-PCR) and Western blotting, and histopathology and tissue injury scores also. The blood was harvested to measure kidney function (creatinine (Cr) and blood urea nitrogen (BUN) levels) after I/R. Cytokines TNF-α, IL-6, HMGB1, and IL-10 were measured after I/R. I/R induced the expression of LC3II, Beclin1, LAMP2, and Rab7. The activation and inhibition of autophagy by rapamycin and 3-MA were promoted and attenuated histological and renal function in renal I/R rats, respectively. Cytokines TNF-α, IL-6, and HMGB1 were decreased, and IL-10 was further increased after activation of autophagy treated in I/R rats, while 3-MA exacerbated the pro-inflammatory cytokines TNF-α, IL-6, HMGB1, and anti-inflammatory cytokine IL-10 in renal I/R. I/R can activated the autophagy, and autophagy increase mitigated the renal injury by decreasing kidney injury score, levels of Cr and BUN after renal I/R, and inflammation response via regulating the balance of pro-inflammation and anti-inflammation cytokines.

Nanoparticle-mediated dual delivery of resveratrol and DAP5 ameliorates kidney ischemia/reperfusion injury by inhibiting cell apoptosis and inflammation

“…There is growing evidence that inflammation erves a key function in acute kidney injury induced by I/R [2, 3, 20]. Our research demonstrated that Res-DAP5-NP decreased the levels of TNF-α, IL-1β, and IL-6 in renal tissue and represents a feasible method to reduce inflammation-related injury.…”

The Role of Autophagy in the Innate Immune Response to Fungal Keratitis Caused by Aspergillus fumigatus Infection

“…37 According to the data from animal researches, increased autophagy can mitigate the renal injury by decreasing the cytokines TNF-α, IL-6, and HMGB1, and upregulating IL-10 to balance the proinflammation and anti-inflammation responses. 38 3-MA and CQ improve the expression of HMGB1, IL-6, and TNF-α, and decrease the production of IL-10 in acute lung injury, whereas treatment with rapamycin can downregulate the levels of HMGB1, IL-6, and TNF-α, and increase the expression of IL-10. 32 The quantification of fungal loads in corneas of mice was increased after 3-MA treatment, whereas CQ or rapamycin decreased the quantification of fungal loads compared with infected control group.…”

Salidroside attenuates neuroinflammation and improves functional recovery after spinal cord injury through microglia polarization regulation

“…Until recently, the function of the autophagy pathway in SCI was unclear. Several recent studies have focused on the usefulness of autophagy as a therapy for inflammation‐induced disease . Increases in the expression levels of autophagic markers have been detected following ischaemia/reperfusion or inflammation injury, indicating that injury or stress can trigger cell self‐protective mechanisms by activating autophagy .…”