Xuezhikang ameliorates contrast media-induced nephropathy in rats via suppression of oxidative stress, inflammatory responses and apoptosis

Chu, Shichun; Hu, Liuhua; Wang, Xiaolei; Sun, Shiqun; Zhang, Tuo; Sun, Zhe; Shen, Linghong; Jin, Shuxuan; He, Ben

doi:10.1080/0886022x.2016.1207052

Cited by 15 publications

(13 citation statements)

References 26 publications

(22 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The apoptotic markers were also reduced [29][30][31][32][33][34]. Furthermore, an appearance of unfavorable histological findings was decreased in an ischemic-reperfusion injury model [29][30][31][32][33][34]. These findings suggested that statins and probucol could attenuate CIN by modulation of NO, inflammatory responses, oxidative stress and apoptotic processes, leading to improved renal function [29][30][31][32][33][34].…”

Section: Lipid-lowering Agents As Interventions To Reduce Cinmentioning

confidence: 82%

“…Lipid-lowering agents including rosuvastatin, [30,31] simvastatin, [31,32] atorvastatin, [31,33] xuezhikang (containing lovastatin), [33] and probucol [34] were investigated as potential pharmacological interventions in CIN animal models. These interventions appeared to effectively attenuate CIN as indicated by decreased level of kidney thiobarbiturates (TBARS), serum or renal MDA, serum protein carbonyl content (PCC), and increased serum thiol and glutathione (GSH) [29][30][31][32][33][34]. Inflammatory markers were also ameliorated as indicated by reduced IL-6, TNF-α, monocyte chemotactic protein-1 (MCP-1), myeloperoxidase (MPO), and increased NO [29][30][31][32][33][34].…”

Section: Lipid-lowering Agents As Interventions To Reduce Cinmentioning

confidence: 99%

“…These interventions appeared to effectively attenuate CIN as indicated by decreased level of kidney thiobarbiturates (TBARS), serum or renal MDA, serum protein carbonyl content (PCC), and increased serum thiol and glutathione (GSH) [29][30][31][32][33][34]. Inflammatory markers were also ameliorated as indicated by reduced IL-6, TNF-α, monocyte chemotactic protein-1 (MCP-1), myeloperoxidase (MPO), and increased NO [29][30][31][32][33][34]. The apoptotic markers were also reduced [29][30][31][32][33][34].…”

Section: Lipid-lowering Agents As Interventions To Reduce Cinmentioning

confidence: 99%

See 2 more Smart Citations

Contrast-induced nephropathy and oxidative stress: mechanistic insights for better interventional approaches

Kusirisin

Chattipakorn

2020

J Transl Med

View full text Add to dashboard Cite

Contrast-induced nephropathy (CIN) or contrast-induced acute kidney injury (CI-AKI) is an iatrogenic acute kidney injury observed after intravascular administration of contrast media for intravascular diagnostic procedures or therapeutic angiographic intervention. High risk patients including those with chronic kidney disease (CKD), diabetes mellitus with impaired renal function, congestive heart failure, intraarterial intervention, higher volume of contrast, volume depletion, old age, multiple myeloma, hypertension, and hyperuricemia had increased prevalence of CIN. Although CIN is reversible by itself, some patients suffer this condition without renal recovery leading to CKD or even end-stage renal disease which required long term renal replacement therapy. In addition, both CIN and CKD have been associated with increasing of mortality. Three pathophysiological mechanisms have been proposed including direct tubular toxicity, intrarenal vasoconstriction, and excessive production of reactive oxygen species (ROS), all of which lead to impaired renal function. Reports from basic and clinical studies showing potential preventive strategies for CIN pathophysiology including low- or iso-osmolar contrast media are summarized and discussed. In addition, reports on pharmacological interventions to reduce ROS and attenuate CIN are summarized, highlighting potential for use in clinical practice. Understanding this contributory mechanism could pave ways to improve therapeutic strategies in combating CIN.

show abstract

Section: Lipid-lowering Agents As Interventions To Reduce Cinmentioning

confidence: 82%

Section: Lipid-lowering Agents As Interventions To Reduce Cinmentioning

confidence: 99%

Section: Lipid-lowering Agents As Interventions To Reduce Cinmentioning

confidence: 99%

See 1 more Smart Citation

Contrast-induced nephropathy and oxidative stress: mechanistic insights for better interventional approaches

Kusirisin

Chattipakorn

2020

J Transl Med

View full text Add to dashboard Cite

show abstract

“…More recently, interest has been raised for the use of NAC in the prevention of cisplatin induced oto- and nephrotoxicity. Interestingly, CIN from iodine-based contrast agents and cisplatin share common mechanistic features including both intrinsic cellular- and inflammation-related ROS mediated cellular and stromal peroxidation damage [ 15 – 20 ]. The following properties of NAC are hypothesized to be paramount for the prevention of oto- and nephrotoxicity: (1) NAC is thought to act as a vasodilator through nitric oxide effects, thus improving blood flow, (2) NAC is a precursor to GSH, the body’s endogenous ROS scavenger, (3) the antioxidant properties of NAC dampen inflammation caused by damage-associated molecular patterns that arise from biological macromolecule peroxidation by ROS and cellular necrosis, and (4) NAC prohibits apoptosis and promotes cell survival by the activation of an extracellular signal-regulated kinase pathway [ 14 ].…”

Section: Introductionmentioning

confidence: 99%

Dose escalation study of intravenous and intra-arterial N-acetylcysteine for the prevention of oto- and nephrotoxicity of cisplatin with a contrast-induced nephropathy model in patients with renal insufficiency

Dósa

Heltai

Radovits

et al. 2017

Fluids Barriers CNS

View full text Add to dashboard Cite

BackgroundCisplatin neuro-, oto-, and nephrotoxicity are major problems in children with malignant tumors, including medulloblastoma, negatively impacting educational achievement, socioemotional development, and overall quality of life. The blood-labyrinth barrier is somewhat permeable to cisplatin, and sensory hair cells and cochlear supporting cells are highly sensitive to this toxic drug. Several chemoprotective agents such as N-acetylcysteine (NAC) were utilized experimentally to avoid these potentially serious and life-long side effects, although no clinical phase I trial was performed before. The purpose of this study was to establish the maximum tolerated dose (MTD) and pharmacokinetics of both intravenous (IV) and intra-arterial (IA) NAC in adults with chronic kidney disease to be used in further trials on oto- and nephroprotection in pediatric patients receiving platinum therapy.MethodsDue to ethical considerations in pediatric tumor patients, we used a clinical population of adults with non-neoplastic disease. Subjects with stage three or worse renal failure who had any endovascular procedure were enrolled in a prospective, non-randomized, single center trial to determine the MTD for NAC. We initially aimed to evaluate three patients each at 150, 300, 600, 900, and 1200 mg/kg NAC. The MTD was defined as one dose level below the dose producing grade 3 or 4 toxicity. Serum NAC levels were assessed before, 5 and 15 min post NAC. Twenty-eight subjects (15 men; mean age 72.2 ± 6.8 years) received NAC IV (N = 13) or IA (N = 15).ResultsThe first participant to experience grade 4 toxicity was at the 600 mg/kg IV dose, at which time the protocol was modified to add an additional dose level of 450 mg/kg NAC. Subsequently, no severe NAC-related toxicity arose and 450 mg/kg NAC was found to be the MTD in both IV and IA groups. Blood levels of NAC showed a linear dose response (p < 0.01). Five min after either IV or IA NAC MTD dose administration, serum NAC levels reached the 2–3 mM concentration which seemed to be nephroprotective in previous preclinical studies.ConclusionsIn adults with kidney impairment, NAC can be safely given both IV and IA at a dose of 450 mg/kg. Additional studies are needed to confirm oto- and nephroprotective properties in the setting of cisplatin treatment. Clinical Trial Registration URL: https://eudract.ema.europa.eu. Unique identifier: 2011-000887-92

show abstract

“…Nowadays, several studies have discovered the antioxidant active constituents from natural plant extracts that could ameliorate CM-induced nephropathy in rats. These agents include magnolin [25], curcumin [7], and xuezhikang [26]. Recently, our previous study showed that pre-treatment with PE extract exhibited the antioxidant effect in CI-AKI rats as shown by the improvement of the oxidative-status parameters including lower renal malondialdehyde, higher renal Total antioxidant capacity (TAC), Superoxide dismutase (SOD) and catalase (CAT) activity, the improved renal function, and the attenuation of the severity of pathological damage [22].…”

Section: Discussionmentioning

confidence: 99%

Protective Effect of Phyllanthus Emblica Extract Prevent Contrast-Induced Acute Kidney Injury in Rats

Kongkham

Tasanarong

Itharat

2019

Asian J Pharm Clin Res

View full text Add to dashboard Cite

Objective: The objective of the study was to investigate the anti-apoptosis effect of the extract from Phyllanthus emblica (PE) for the prevention of contrast-induced acute kidney injury (CI-AKI). Methods: Male Sprague Dawley rats were given saline (control) or PE extracts (500 mg/kg/day) for 5 days before the induction of CI-AKI. Renal tissues were collected for an evaluation of gene expression and immunohistochemistry (IHC). To indicate anti-apoptotic effect, the expression levels of Bax, Bcl-2, and caspase in kidney were also determined, using real-time polymerase chain reaction (RT-PCR) and Western blot analysis. Results: In the CI-AKI group, RT-PCR and Western blot analysis revealed that the expression levels of Bax and cleaved-caspase-3 were upregulated in the CI-AKI group, whereas the expression of Bcl-2 was downregulated. However, the pre-treatment with PE increased Bcl-2 expression. Moreover, decreased cleaved-caspases-3 activity was also detected using IHC. Conclusion: These findings suggested that pretreatment with PE extract provided the anti-apoptotic effect against CI-AKI in the rat model.

show abstract

Xuezhikang ameliorates contrast media-induced nephropathy in rats via suppression of oxidative stress, inflammatory responses and apoptosis

Cited by 15 publications

References 26 publications

Contrast-induced nephropathy and oxidative stress: mechanistic insights for better interventional approaches

Contrast-induced nephropathy and oxidative stress: mechanistic insights for better interventional approaches

Dose escalation study of intravenous and intra-arterial N-acetylcysteine for the prevention of oto- and nephrotoxicity of cisplatin with a contrast-induced nephropathy model in patients with renal insufficiency

Protective Effect of Phyllanthus Emblica Extract Prevent Contrast-Induced Acute Kidney Injury in Rats

Contact Info

Product

Resources

About