Abstract
Background: Anethole is the principle essential oil component of anise and fennel. Renal ischemia/reperfusion (RIR) is one of the utmost imperative reasons for acute kidney injury and often associated with high mortality rate. The aim of this study is to investigate the protective effect of anethole on RIR status, exploring the involved mechanisms. Methods: RIR was accomplished by bilateral renal pedicle clamping for 45 min, after which the clamps were removed to achieve the reperfusion phase. Rats were randomized into five groups; Sham, Sham + anethole, RIR, and finally RIR + anethole (125 mg/kg or 250 mg/kg) groups. Animals were given anethole (in specified groups in doses) for 14 days before RIR. Results: RIR-experienced animals developed renal injury evidenced by diminished renal function and histopathological alteration. RIR induced severe oxidative, inflammatory, and apoptotic status within renal tissue. Pre-RIR management with anethole enhanced renal morphology and improved renal function. Anethole amplified GSH content and SOD, CAT, and GPx activities and lowered MDA. Anethole reduced gene and protein expression levels of HMGB1, TLR2, TLR4, MYD88, and NFκB. Anethole distinctly dropped TNF-α, IFN-γ, and MCP-1 levels, increased IL-10, and diminished caspase 3 and 9, reflecting its anti-inflammatory and anti-apoptotic actions. Conclusion: Anethole displayed anti-inflammatory, anti-oxidant, and anti-apoptotic actions against RIR-induced injury. Anethole exhibited renal protective actions, which could be through inhibiting the HMGB1/TLR2, 4/MYD88/NFκB pathway. These results could suggest anethole as a protective agent against RIR.
Highlights
Introduction distributed under the terms and During certain clinical settings such as renal transplant, hemi-nephrectomy, and renal artery occlusion, renal blood supply is temporarily declined or even impaired, causing renal ischemia/reperfusion (RIR) injury [1]
As for the IHC analysis, the results revealed that NFκB (Figure 6a) and HMGB1 (Figure 6b) positive cells were infrequently present in the sham animals
HMGB1 and NFκB positive cells were lowered in animal groups pretreated with anethole compared with the RIR group (p < 0.05). These results provide evidence that reno-protective effects of anethole could be via the inhibition of the HMGB1/TLR2, 4/myeloid differentiation primary response gene 88 (MYD88)/NFκB pathway
Summary
Introduction distributed under the terms andDuring certain clinical settings such as renal transplant, hemi-nephrectomy, and renal artery occlusion, renal blood supply is temporarily declined or even impaired, causing renal ischemia/reperfusion (RIR) injury [1]. RIR is one of the highest imperative reasons for acute kidney injury and mortality [2]. RIR injury involves oxidative stress [3], inflammation [4], conditions of the Creative Commons. Oxygen-derived free radical intensification outweighs renal detoxification capability, leading to lipid peroxidation as well as cellular membrane destruction [3]. This process prompts pro-inflammatory reactions, leading to renal cells apoptosis. Renal ischemia/reperfusion (RIR) is one of the utmost imperative reasons for acute kidney injury and often associated with high mortality rate. RIR + anethole (125 mg/kg or 250 mg/kg) groups. Animals were given anethole (in specified groups in doses) for 14 days before RIR. Results: RIR-experienced animals developed renal injury evidenced by diminished renal function and histopathological alteration. Anethole distinctly dropped TNF-α, IFN-γ, and MCP-1 levels, increased
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