Neuroprotective effect of preadministration with Ganoderma lucidum spore on rat hippocampus

Zhou, Yan; Qu, Ze-qiang; Zeng, Yuan-Shan; Lin, Yukun; Li, Yan; Chung, Peter; Wong, Ricky W.K.; Hägg, Urban

doi:10.1016/j.etp.2010.12.011

Cited by 57 publications

(43 citation statements)

References 48 publications

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“…In addition, the potential use of this fungus for the treatment of neurological diseases has also been examined. It was shown that long-term consumption of G. lucidum can decrease the progression of Alzheimer's disease (Lai et al, 2008;Zhou et al, 2012). This observed neuroprotective effect is achieved by promotion of neuritogenesis and reduction of senescence of the neurons (Ling-Sing Seow et al, 2013).…”

Section: Effect On Lower Urinary Tract Symptoms In Menmentioning

confidence: 94%

From 2000years of Ganoderma lucidum to recent developments in nutraceuticals

et al. 2015

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Section: Effect On Lower Urinary Tract Symptoms In Menmentioning

confidence: 94%

From 2000years of Ganoderma lucidum to recent developments in nutraceuticals

et al. 2015

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“…Growing lines of evidence suggests that preadministration with Ganoderma lucidum spore may show neuroprotective effect against oxidative impairment and perturbation of energy metabolism in hippocampus of streptozotocin induced Sprague-Dawley rats [115]. This may open a new therapeutic avenue for AD.…”

Section: Natural Compoundsmentioning

confidence: 98%

Apoptosis in Alzheimer’s Disease: An Understanding of the Physiology, Pathology and Therapeutic Avenues

2014

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Alzheimer's disease (AD) is a devastative neurodegenerative disorder with complex etiology. Apoptosis, a biological process that plays an essential role in normal physiology to oust a few cells and contribute to the normal growth, when impaired or influenced by various factors such as Bcl2, Bax, caspases, amyloid beta, tumor necrosis factor-α, amyloid precursor protein intracellular C-terminal domain, reactive oxygen species, perturbation of enzymes leads to deleterious neurodegenerative disorders like AD. There are diverse pathways that provoke manifold events in mitochondria and endoplasmic reticulum (ER) to execute the process of cell death. This review summarizes the crucial apoptotic mechanisms occurring in both mitochondria and ER. It gives substantial summary of the diverse mechanisms studied in vivo and in vitro. A brief account on neuroprotection of several bioactive components, flavonoids and antioxidants of plants against apoptotic events of both mitochondria and ER in both in vitro and in vivo has been discussed. In light of this, the burgeoning need to develop animal models to study the efficacy of various therapeutic effects has been accentuated.

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“…It is well reported that central STZ administration (3 mg/kg) produces morphological and histological changes within 3 weeks in rat brain that further results in learning and memory impairment (Shoham et al, 2003;Ishrat et al, 2009;Saxena et al, 2010;Zhou et al, 2011). Although, the present study focused on neurons in the hippocampal area that are relevant to cognitive dysfunction and emphasized the role of COX isozymes in such dysfunction, however, enlargement of ventricle, increased macrophages and activated microglia are part of neuroinflammation during ICV-STZ induced neurodegeneration has been well studied (Shoham et al, 2003(Shoham et al, , 2007.…”

Section: Discussionmentioning

confidence: 99%