Chlorogenic Acid Attenuates Lipopolysaccharide-Induced Acute Kidney Injury by Inhibiting TLR4/NF-κB Signal Pathway

Abstract

Chlorogenic acid (CGA), a polyphenolic compound, exists widely in medicinal herbs, which has been shown a strong antioxidant and anti-inflammatory effect. This study investigated the protective effects and mechanism of CGA on lipopolysaccharide (LPS)-induced acute kidney injury (AKI). Treatment of CGA successfully ameliorates LPS-induced renal function and pathological damage. Moreover, CGA dose-dependently suppressed LPS-induced blood urea nitrogen (BUN), creatinine levels, and inflammatory cytokines TNF-α, IL-6, and IL-1β in serum and tissue. The relative proteins' expression of TLR4/NF-κB signal pathway was assessed by western blot analysis. Our results showed that CGA dose-dependently attenuated LPS-induced kidney histopathologic changes, serum BUN, and creatinine levels. CGA also suppressed LPS-induced TNF-α, IL-6, and IL-1β production both in serum and kidney tissues. Furthermore, our results showed that CGA significantly inhibited the LPS-induced expression of phosphorylated NF-κB p65 and IκB as well as the expression of TLR4 signal. In conclusion, our results provide a mechanistic explanation for the anti-inflammatory effects of CGA in LPS-induced AKI mice through inhibiting TLR4/NF-κB signaling pathway.

LncRNA TapSAKI promotes inflammation injury in HK-2 cells and urine derived sepsis-induced kidney injury

“…observed that inhibition of TLR4/NF‐κB pathway could reduce inflammatory response and urine derived sepsis‐induced kidney injury. Lipopolysaccharide is a classical ligand for TLR4 that can activate TLR4‐/NF‐κB signaling pathway in acute kidney injury mice, which leads to the increase of inflammatory cytokine, such as interleukin‐6 (IL‐6) and tumor necrosis factor‐α (TNF‐α) . PTEN also involved in LPS induced proinflammatory cytokine production .…”

“…Lipopolysaccharide is a classical ligand for TLR4 that can activate TLR4-/NF-jB signaling pathway in acute kidney injury mice, which leads to the increase of inflammatory cytokine, such as interleukin-6 (IL-6) and tumor necrosis factor-a (TNF-a). [12] PTEN also involved in LPS induced proinflammatory cytokine production. [13] Therefore, PTEN and TLR4/NF-jB pathway play important role in urine derived sepsis-induced kidney injury.…”

Chlorogenic acid alleviates sepsis-induced endothelial barrier dysfunction and the underlying mechanism

“…Previous studies have shown that CGA protects against vital organ injury, such as acute liver and acute kidney injury, by inhibiting inflammasome activation. 18,19 The present study showed that CGA significantly improved vascular leakage in septic shock rats, then enhanced tissue perfusion in vital organs including the heart, and thus improved hemodynamic status and survival time. Improvement in the endothelial barrier by CGA was closely related to increased expression of ZO-1 and VEcadherin.…”

The Regulation of Host Intestinal Microbiota by Polyphenols in the Development and Prevention of Chronic Kidney Disease

“…C-QA protects liver and kidney injury in mice caused by D-galactose, due to C-QA's antioxidation and anti-inflammation effects (110). C-QA also attenuates AKI caused by LPS by inhibiting the TLR4/NF-κB signaling pathway (107). The results of this study indicated that C-QA decreased LPS-induced kidney damage by suppressing oxidative stress, inflammation, apoptosis and autophagy, enhancing kidney regeneration (111).…”