Lithium improves the behavioral disorder in rats subjected to transient global cerebral ischemia

Yan, Xinfeng; Wang, Shanshan; Hou, Hailong; Ji, Rui; Zhou, Jiang‐Ning

doi:10.1016/j.bbr.2006.11.021

Cited by 79 publications

(36 citation statements)

References 44 publications

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“…The cellular mechanisms underlying lithium's protective effects are not completely understood, and two independent aspects may be involved: the prevention of apoptotic cell death (Chen and Chuang, 1999;Li et al, 2010) and the stimulation of compensatory neurogenesis/cell migration (Su et al, 2007). Early after ischemia, lithium may reduce apoptotic death to diminish abnormal behavioral performance (Ren et al, 2003;Xu et al, 2003;Yan et al, 2007b). At later stages, increased generation and survival of newborn cells in the neurogenic regions may also contribute to the beneficial effects of lithium (Su et al, 2007(Su et al, , 2009.…”

Section: Discussionmentioning

confidence: 99%

Lithium-Mediated Long-Term Neuroprotection in Neonatal Rat Hypoxia–Ischemia is Associated with Antiinflammatory Effects and Enhanced Proliferation and Survival of Neural Stem/Progenitor Cells

et al. 2011

J Cereb Blood Flow Metab

103

112

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The aim of this study was to evaluate the long-term effects of lithium treatment on neonatal hypoxicischemic brain injury, inflammation, and neural stem/progenitor cell (NSPC) proliferation and survival. Nine-day-old male rats were subjected to unilateral hypoxia-ischemia (HI) and 2 mmol/kg lithium chloride was injected intraperitoneally immediately after the insult. Additional lithium injections, 1 mmol/kg, were administered at 24-hour intervals for 7 days. Animals were killed 6, 24, 72 hours, or 7 weeks after HI. Lithium reduced total tissue loss by 69%, from 89.4 ± 14.6 mm 3 in controls (n = 15) to 27.6 ± 6.2 mm 3 in lithium-treated animals (n = 14) 7 weeks after HI (P < 0.001). Microglia activation was inhibited by lithium treatment, as judged by Iba-1 and galectin-3 immunostaining, and reduced interleukin-1b and CCL2 levels. Lithium increased progenitor, rather than stem cell, proliferation in both nonischemic and ischemic brains, as judged by 5-bromo-2-deoxyuridine labeling 24 and 72 hours as well as by phospho-histone H3 and brain lipid-binding protein labeling 7 weeks after HI. Lithium treatment also promoted survival of newborn NSPCs, without altering the relative levels of neuronal and astroglial differentiation. In summary, lithium conferred impressive, morphological long-term protection against neonatal HI, at least partly by inhibiting inflammation and promoting NSPC proliferation and survival.

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Section: Discussionmentioning

confidence: 99%

Lithium-Mediated Long-Term Neuroprotection in Neonatal Rat Hypoxia–Ischemia is Associated with Antiinflammatory Effects and Enhanced Proliferation and Survival of Neural Stem/Progenitor Cells

et al. 2011

J Cereb Blood Flow Metab

103

112

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“…11 Lithium has been well known to have a potent promotional effect on tissue repair and regeneration after injury in multiple organ systems, including the central nervous system and hematopoietic system, [12][13][14][15] whereas the effect of lithium on kidney repair and renal recovery after AKI is unknown. This study examined the effect of delayed administration of a single low dose of lithium on a murine model of cisplatin or ischemia/reperfusion-induced AKI.…”

mentioning

confidence: 99%

Delayed Administration of a Single Dose of Lithium Promotes Recovery from AKI

Bao

Wang

et al. 2014

Journal of the American Society of Nephrology

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Evidence suggests that glycogen synthase kinase 3b (GSK3b) contributes to AKI; however, its role in post-AKI kidney repair remains uncertain. Here, delayed treatment with a single dose of lithium, a selective inhibitor of GSK3b and a US Food and Drug Administration-approved mood stabilizer, accelerated recovery of renal function, promoted repopulation of renal tubular epithelia, and improved kidney repair in murine models of cisplatin-and ischemia/reperfusion-induced AKI. These effects associated with reduced GSK3b activity and elevated expression of proproliferative molecules, including cyclin D1, c-Myc, and hypoxia-inducible factor 1a (HIF-1a), in renal tubular epithelia. In cultured renal tubular cells, cisplatin exposure led to transient repression of GSK3b activity followed by a prolonged upregulation of activity. Rescue treatment with lithium inhibited GSK3b activity, enhanced nuclear expression of cyclin D1, c-Myc, and HIF-1a, and boosted cellular proliferation. Similarly, ectopic expression of a kinase-dead mutant of GSK3b enhanced the expression of cyclin D1, c-Myc, and HIF-1a and amplified cellular proliferation after cisplatin injury, whereas forced expression of a constitutively active mutant of GSK3b abrogated the effects of lithium. Mechanistically, GSK3b colocalized and physically interacted with cyclin D1, c-Myc, and HIF-1a in tubular cells. In silico analysis revealed that cyclin D1, c-Myc, and HIF-1a harbor putative GSK3b consensus phosphorylation motifs, implying GSK3b-directed phosphorylation and subsequent degradation of these molecules. Notably, cotreatment with lithium enhanced the proapoptotic effects of cisplatin in cultured colon cancer cells. Collectively, our findings suggest that pharmacologic targeting of GSK3b by lithium may be a novel therapeutic strategy to improve renal salvage after AKI.

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“…When taste axons arrive at the lingual epithelium taste bud regeneration is initiated, and both taste bud and cell number increase Guagliardo and Hill 2007;Robinson 1989). The degree of anatomical regeneration also varies among species, Guagliardo and Hill 2007;Montavon et al 1996;Robinson 1989;Yan et al 2007). Specifically, in gerbil, less than 2 weeks after chorda tympani nerve section, some taste fibers regenerated into the tongue and taste bud number and size increased progressively .…”

Section: Regeneration Of Taste System Following Gustatory Nerve Sectimentioning

confidence: 96%

Role of neurotrophin in the taste system following gustatory nerve injury

Meng

Jiang

2014

Metab Brain Dis

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Taste system is a perfect system to study degeneration and regeneration after nerve injury because the taste system is highly plastic and the regeneration is robust. Besides, degeneration and regeneration can be easily measured since taste buds arise in discrete locations, and nerves that innervate them can be accurately quantified. Neurotrophins are a family of proteins that regulate neural survival, function, and plasticity after nerve injury. Recent studies have shown that neurotrophins play an important role in the developmental and mature taste system, indicating neurtrophin might also regulate taste system following gustatory nerve injury. This review will summarize how taste system degenerates and regenerates after gustatory nerve cut and conclude potential roles of neurotrophin in regulating the process.

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Lithium improves the behavioral disorder in rats subjected to transient global cerebral ischemia

Cited by 79 publications

References 44 publications

Lithium-Mediated Long-Term Neuroprotection in Neonatal Rat Hypoxia–Ischemia is Associated with Antiinflammatory Effects and Enhanced Proliferation and Survival of Neural Stem/Progenitor Cells

Lithium-Mediated Long-Term Neuroprotection in Neonatal Rat Hypoxia–Ischemia is Associated with Antiinflammatory Effects and Enhanced Proliferation and Survival of Neural Stem/Progenitor Cells

Delayed Administration of a Single Dose of Lithium Promotes Recovery from AKI

Role of neurotrophin in the taste system following gustatory nerve injury

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