Atorvastatin attenuates experimental contrast-induced acute kidney injury: a role for TLR4/MyD88 signaling pathway

Yue, Rongzheng; Zuo, Chuantao; Zeng, Jing; Su, Baihai; Tao, Ye; Huang, Songmin; Zeng, Rui

doi:10.1080/0886022x.2017.1361838

Cited by 19 publications

(16 citation statements)

References 27 publications

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“…This study proves that, after CT examination, the incidence of CI‐AKI in the control group is 8%, and that in the observation group is 2%. It is suggested that the use of intensive dose of atorvastatin can effectively reduce the incidence of AKI, which is consistent with the research results reported abroad 20–22 23,24 …”

Section: Discussionsupporting

confidence: 89%

“…25,26 CysC is more sensitive and accurate than SCR and BUN, and it can be used as one of the diagnostic criteria for early renal function damage. 22,27,28 eGFR is more accurate, stable, and comprehensive than CysC, SCR, and BUN in the evaluation of renal function, and it is the most commonly used evaluation index of renal function. 29,30 The values of eGFR were significantly decreased in the control group, but were almost no change in the observation group, indicating that the intensive dose of atorvastatin has a certain protective effect on renal function as indicated as the changes of the levels of SCR, CysC, BUN, and eGFR.…”

Section: Discussionmentioning

confidence: 99%

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The preventive effects of different doses of atorvastatin on contrast‐induced acute kidney injury after CT perfusion

Yan

Gao

Yang

et al. 2022

Clinical Laboratory Analysis

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Background: Contrast-induced acute kidney injury (CI-AKI) is a severe complication among patients receiving intravascular contrast media. The purpose of this study was to investigate the preventive effects of pretreatment of atorvastatin at intensive doses on CI-AKI after computed tomography (CT) perfusion. Methods:The levels of serum creatinine (SCR), blood urea nitrogen (BUN), Cystatin C (CysC), estimated glomerular filtration rate (eGFR), high-sensitivity C-reactive protein (hs-CRP), and interleukin-6 (IL-6) in patients were compared between the observation group receiving 40 mg/kg atorvastatin and the control group receiving 20 mg/ kg atorvastatin before and 72 h after CT examination. In addition, the incidence of CI-AKI was recorded.Results: Compared with the control group, the incidence of renal injury in the observation group was significantly reduced, from 8% to 2% (χ 2 = 6.62, p = 0.010). In addition, there was no notable difference in the levels of Scr, BUN, CysC, hs-CRP, and IL-6 before CT examination between two groups (p > 0.05). The levels of SCR, BUN, CysC, hs-CRP, and IL-6 were increased, while the levels of eGFR were decreased in the control group at 72 h after CT examination (p < 0.05). At 72 h after CT enhancement, the levels of BUN, CysC, and hs-CRP were prominently increased in the observation group (p < 0.05), while SCR, eGFR, and IL-6 did not change (p > 0.05). Compared with the control group, the levels of SCR, BUN, CysC, eGFR, hs-CRP, and IL-6 in the observation group were significantly decreased at 72 h after CT examination (p < 0.05). Conclusion:Intensive dose of atorvastatin pretreatment can prevent CI-AKI undergoing CT perfusion through lowering inflammation as well as renal function indexes SCR, CysC, BUN, and eGFR.

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Section: Discussionsupporting

confidence: 89%

Section: Discussionmentioning

confidence: 99%

The preventive effects of different doses of atorvastatin on contrast‐induced acute kidney injury after CT perfusion

Yan

Gao

Yang

et al. 2022

Clinical Laboratory Analysis

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“…Renal tissues affected by high osmotic load could make intense focal or diffuse vacuolization of the proximal tubules or overt tubular necrosis appear ( 20 ). Statins attenuate CIN through modulation of inflammation and endothelial function, besides reducing oxidative stress and apoptosis ( 21 - 23 ).…”

Section: Discussionmentioning

confidence: 99%

Efficacy of short-term moderate or high-dose statin therapy for the prevention of contrast-induced nephropathy in high-risk patients with chronic kidney disease: systematic review and meta-analysis

Zhou¹,

Chen²,

Du³

2021

Clinics

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“…Similarly, NF-κB is aberrantly activated in CIN, but NF-κB expression is decreased and renal tissue hyalinization, hemorrhagic casts, and necrosis are reduced after infliximab treatment (Saritemur et al, 2015). And TLR4/Myd88/NF-κB is also involved in the protective pathway (Yue et al, 2017). In addition, a study has revealed that overexpression of miR429 inhibits the NF-κB signaling pathway by targeting programmed cell death 4 (PDCD4) to reduce apoptosis and improve cell viability in a CI-AKI cell model (Niu et al, 2021).…”

Section: Contrast-induced (Ci) Akimentioning

confidence: 99%

Dissecting the Crosstalk Between Nrf2 and NF-κB Response Pathways in Drug-Induced Toxicity

Gao

Guo

Yang

et al. 2022

Front. Cell Dev. Biol.

115

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Nrf2 and NF-κB are important regulators of the response to oxidative stress and inflammation in the body. Previous pharmacological and genetic studies have confirmed crosstalk between the two. The deficiency of Nrf2 elevates the expression of NF-κB, leading to increased production of inflammatory factors, while NF-κB can affect the expression of downstream target genes by regulating the transcription and activity of Nrf2. At the same time, many therapeutic drug-induced organ toxicities, including hepatotoxicity, nephrotoxicity, cardiotoxicity, pulmonary toxicity, dermal toxicity, and neurotoxicity, have received increasing attention from researchers in clinical practice. Drug-induced organ injury can destroy body function, reduce the patients’ quality of life, and even threaten the lives of patients. Therefore, it is urgent to find protective drugs to ameliorate drug-induced injury. There is substantial evidence that protective medications can alleviate drug-induced organ toxicity by modulating both Nrf2 and NF-κB signaling pathways. Thus, it has become increasingly important to explore the crosstalk mechanism between Nrf2 and NF-κB in drug-induced toxicity. In this review, we summarize the potential molecular mechanisms of Nrf2 and NF-κB pathways and the important effects on adverse effects including toxic reactions and look forward to finding protective drugs that can target the crosstalk between the two.

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Atorvastatin attenuates experimental contrast-induced acute kidney injury: a role for TLR4/MyD88 signaling pathway

Abstract: Different atorvastatin doses have protective effects on contrast-induced acute renal tubular injury in rats, possibly by targeting TLR4, suppressing TLR4 expression, regulating the TLR4/Myd88 signaling pathway, and inhibiting the expression of downstream inflammatory factors.

Cited by 19 publications

References 27 publications

The preventive effects of different doses of atorvastatin on contrast‐induced acute kidney injury after CT perfusion

The preventive effects of different doses of atorvastatin on contrast‐induced acute kidney injury after CT perfusion

Efficacy of short-term moderate or high-dose statin therapy for the prevention of contrast-induced nephropathy in high-risk patients with chronic kidney disease: systematic review and meta-analysis

Dissecting the Crosstalk Between Nrf2 and NF-κB Response Pathways in Drug-Induced Toxicity

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