Protective Activities of Scutellarin against Alcohol‐Induced Acute Kidney Injury

Abstract

Acute alcohol consumption has adverse effects in the kidney, resulting in kidney damage and disease, which are typically accompanied by oxidation and inflammation. Scutellarin (SCU) is the major effective ingredient of breviscapine and its anti-inflammation and antioxidant efficacy has been previously reported. The present study revealed the protective effective of SCU as therapeutic medicine against alcohol-induced inflammation and oxidative stress, leading to acute kidney injury (AKI). The AKI model was established by giving 50 % ethanol (12 mL/kg) via lavage. Kidney tissues were collected and used for histopathology analysis, biochemical assays and qRT-PCR analysis. The therapeutic effects of SCU were evaluated by observing pathological changes from HE-stained kidney tissues. Additionally, the anti-inflammation activity of SCU was evaluated by measuring the relative mRNA expression levels of Tnf-α, Il-1β, Il-6 and the activity of iNOS. The antioxidant capacity was assessed by measuring the lipid peroxidation marker 'MDA' and antioxidant enzymes activity of SOD, CAT and GSH-Px. The results showed that serious swelling and damage occurred in the renal tubular epithelium of alcohol intake group, accompanying with glomerular atrophy, necrosis and increase of inflammatory infiltration. SCU treatment significantly reduced the damage of diseased renal tubular epithelium and glomerular, and less inflammatory cell emerged. The inflammation cytokines expression levels were elevated and oxidative stress index decreased after alcohol intake compared to the control group. In conclusion, inflammation and oxidative stress occur in the kidney after acute and excessive alcohol intake, SCU exhibited protective roles via its anti-inflammation and antioxidant activity in AKI.

Nephroprotective Efficacy of Echinops spinosus against a Glycerol-Induced Acute Kidney Injury Model

“…These results were confirmed by Hegazy et al as they measured the effect of ES on induced renal inflammation. Finally, these oxidative stress and inflammatory mediators help each other and start damaging the kidney tissue, forming AKI . According to the findings, in our case, renal stimulation using glycerol enhanced the proinflammatory cytokine release via overproduction of both renal TNF-α and IL-1β.…”

“…Finally, these oxidative stress and inflammatory mediators help each other and start damaging the kidney tissue, forming AKI. 2 According to the findings, in our case, renal stimulation using glycerol enhanced the proinflammatory cytokine release via overproduction of both renal TNF-α and IL-1β. Studies have demonstrated that active components found in ESE inhibited the synthesis of TNF-α as well as the creation of IL-1β.…”

“…Acute kidney injury (AKI), commonly known as a “kidney attack”, is a sudden and unexpected decline in kidney function that has an unclear incidence and effect and can occur in the community or during hospitalization. Serious complication leads patients to an intensive care unit (ICU), particularly the elderly. , Another way to describe AKI is if the serum creatinine (sCr) level has increased by 1.5 times from baseline (within 48 h to the previous 7 days) or by an absolute amount above 0.5 mg/dL (44.2 mol/L), or if the urine volume has decreased to less than 0.5 mL/kg/h for at least 6 h. , Many factors can lead to AKI, especially alcohol, diabetes, cardiac dysfunction, volume depletion, and hepatic failure. , AKI can be caused by a variety of factors, including acute tubular necrosis, renal ischemia-reperfusion, drug-induced acute interstitial glomerulonephritis or nephrotoxicity, infection, and hepatorenal syndrome. , …”

“…AKI pathophysiology is complex and multifactorial, characterized by intrarenal hemodynamic changes, oxidation, endothelial dysfunction, inflammation, intraglomerular thrombosis, and tubule obstruction with necrotic cells and debris. The cases of AKI worsen in different medical situations, such as volume depletion, hypoalbuminemia, and in the presence of acidic urine. ,, Also, AKI is distinguished by renal tubular injury and rhabdomyolysis (leakage of skeletal muscle fiber content into the blood, resulting in myoglobin buildup in renal tubules). Between 10 and 50% of rhabdomyolysis patients get some degree of AKI .…”

Scutellarin ameliorates diabetic nephropathy via TGF-β1 signaling pathway

“…These effects suggest that the injection of breviscapine benefit to patients with DN. In addition, Scutellarin has been reported to protect against kidney injury [ 27 – 30 ] via its anti-inflammation and antioxidant activity.…”