2013
DOI: 10.1016/j.toxlet.2013.04.023
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Nephroprotective effect of GSK-3β inhibition by lithium ions and δ-opioid receptor agonist dalargin on gentamicin-induced nephrotoxicity

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Cited by 31 publications
(21 citation statements)
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“…The initial target of ACR appears to be nerve terminals in both the central and peripheral nervous systems, resulting in autonomic, behavioral, sensory, and motor disturbances [27]. Interestingly, lithium enhances cytoskeleton stability and axonal transport, promotes neurite outgrowth, and increases axonal growth rate [17,28,29]. In consistent with previously studies [30], we found that mice receiving ACR resulted in hind-limb paralysis and walking difficulties.…”
Section: Discussionsupporting
confidence: 88%
“…The initial target of ACR appears to be nerve terminals in both the central and peripheral nervous systems, resulting in autonomic, behavioral, sensory, and motor disturbances [27]. Interestingly, lithium enhances cytoskeleton stability and axonal transport, promotes neurite outgrowth, and increases axonal growth rate [17,28,29]. In consistent with previously studies [30], we found that mice receiving ACR resulted in hind-limb paralysis and walking difficulties.…”
Section: Discussionsupporting
confidence: 88%
“…10,11 In contrast to these adverse effects of lithium treatment, accumulating evidence suggests that the administration of low lithium amounts (,0.6 mM in blood) improves kidney function in different animal nephropathy models. Single-bolus injections or short-term treatment (,1 week) of lithium reduced adriamycin-, LPS-, cisplatin-, gentamicin-, and ischemiainduced AKI, [12][13][14][15][16][17][18] whereas prolonged treatment ($1 month) alleviated kidney damage because of ischemia-reperfusion, hypertension, and the autoimmune disease lupus erythematosus. [19][20][21] To understand these opposing findings, we will first present an overview of renal lithium handling and then, discuss the molecular pathways underlying the toxic and potential therapeutic effects of lithium in the kidney.…”
mentioning
confidence: 99%
“…After 24-hour reperfusion, serum creatinine was significantly increased and the high level of serum creatinine was maintained at 48 hours, suggesting that kidney injury, and not repair or recovery, still predominated. 10 Therefore, the protective effects of lithium on renal function and tubular damage could be the result of suppressing cell death, as suggested by other studies, [6][7][8][9] and not the result of promoting cell proliferation and regeneration. The effect of lithium on renal recovery in ischemic AKI should be better observed within a reperfusion period.48 hours to ensure that the recovery does occur.…”
mentioning
confidence: 87%
“…5 In stark contrast, if used briefly and at low doses, lithium can be renoprotective. In this regard, recent studies have shown the protective effects of lithium in experimental models of AKI induced by renal ischemia-reperfusion, 6,7 nephrotoxin, 8 and endotoxin. 9 In this issue of JASN, Bao et al report that a single dose of lithium given after AKI promotes the recovery and repair of kidneys, whereas de Groot and colleagues show that lithium induces G2 cell cycle arrest in the principal cells of the collecting ducts, which may contribute to the development of NDI.…”
mentioning
confidence: 99%
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