Icariside II in Neurological Disorders: Mechanistic Insights Into Alzheimer's Disease, Cerebral Ischemia and Parkinson's Disease.
Icariside II in Neurological Disorders: Mechanistic Insights Into Alzheimer's Disease, Cerebral Ischemia and Parkinson's Disease.
Where did the research take place?
Possible study sites were matched from the text; these need review.
Most, CZ · Possible study site
Most studies have been conducted using rodent models or in vitro cell lines, particularly Aβ‐induced models, which primarily reproduce amyloid‐related pathology but does not cover the complex and multifactorial pathology of human AD, including tau pathology, chronic neurodegeneration, and age‐associated disease progression.Location evidence
Noida, IN · Author affiliation
Department of Pharmacology, College of Pharmacy, JSS University, Noida, Uttar Pradesh, India.Location evidence
Anand, IN · Author affiliation
Anand College of Pharmacy, SGI, Agra, Uttar Pradesh, India.Location evidence
Agra, IN · Author affiliation
Anand College of Pharmacy, SGI, Agra, Uttar Pradesh, India.Location evidence
Mathura, IN · Author affiliation
Division of Pharmacology, Institute of Pharmaceutical Research, GLA University, Mathura, Uttar Pradesh, India.Location evidence
A plain-language reading has not been prepared for this paper yet.
Original abstract
Icariside II (ICS II), a PDE5 inhibitor, is a flavonoid glycoside and primary metabolite of icariin, derived from the herb Herba epimedii, and exhibits promising neuroprotective potential in various pre-clinical studies. The current review provides evidence that ICS II shows neuroprotective potential against various neurological disorders, mainly including Alzheimer's disease, Parkinson's disease and Cerebral ischemia through modulating neuroinflammation, oxidative stress, neural apoptosis, neurogenesis, mitochondrial and cognitive dysfunction. It regulates multiple signalling pathways including PI3K/Akt, Keap1/Nrf2, TLR4/MyD88/NF-κB, cGMP/PKG/CREB, TGFB1/Smad, Wnt/β-catenin signaling and BDNF/TrkB/CREB. The pre-clinical evidence suggests that ICS II attenuates oxidative stress through increasing antioxidant enzymes SOD, GSH, catalase, and HO-1, with decreasing MDA and lipid peroxidation. Neuroinflammation is suppressed by inhibition of pro-inflammatory cytokines and down-regulation of IL-1β, IL-6, TNF-α, COX-2, iNOS levels and up-regulation of tight-junction proteins like occludin, claudin-5, ZO-1. Apoptosis is regulated via altering PARP, Bcl-2, Bax/Bcl-2 ratio and reducing caspase-3 activation. Mitochondrial dysfunction is ameliorated by restoring Complex I activity and increasing mitofusin-1/2 expression and reducing mitochondrial fission factors. Collectively, these molecular mechanisms show promise for ICS II as a potential candidate in different in vivo and in vitro studies of neurological disorders.