NEUROPROTECTIVE AGENTS, NATURAL PLANT HERBS & DRUGS IN ISCHEMIC STROKE: A REVIEW

Drug

Dose

Model

Parameters

Result

Pravastatin

1 mg/kg

BCCAO for 8 min.

In Situ Apoptosis Detection, Western blotting.

The proportion of viable neuronal cells after ischemia was greater in the pravastatin vs. control group, with greater expression of apoptotic cells in the control vs. pravastatin group. Bax protein expression was significantly decreased whereas, Bcl-2 expression was increased, but not significantly[17].

Senkyunolide I

36  and 72 mg/kg

MCAO

Neurological function assessment, Measurement of brain water content, Detection of reporter gene activity

SEI administration significantly ameliorated the neurological deficit, reduced the infarct volume and brain edema, reversed the cerebralmorphologicdamage,decreasedthelevels of MDA and increased the activities of superoxide dismutase [25].

Phloretin

20, 40, and 80 mg/kg

MCAO

Determination of SOD, GSH, glutathione peroxidase, and MDA levels, Reverse transcription polymerase chain reaction (RT-PCR), Western blot analysis

Phloretin significantly reduced infarct volume, brain edema, and ameliorated neurological scores. SOD, GSH and GSH-Px activities were greatly decreased, and MDA levels significantly increased. However, phloretin pretreatment dramatically suppressed these oxidative stress processes. Furthermore, phloretin up regulated Nrf2 mRNA and protein expression [26].

Mgso4

1 mmol/kg

BCCAO for 10-min   reperfusion 72 hr

Mitochondrial isolation and AFM measurement, Nissl staining

The MgSO4 reduced the perimeter of ischemic mitochondria. The length, width and area were significantly different. Besides, the adhesion force of isolated mitochondria from the MgSO4 group was close[27].

 

 

 

 

HAMI 3379

0.025, 0.05, 0.1, 0.2 and 0.4 mg/kg

MCAO for 60 min,24 or 72 hr reperfusion

Behavioural parameters Inclined board test Biochemical parameter-

Cytokine assay

It attenuated the neurological deficits, and reduced infarct volume, brain edema, and neuronal loss and degeneration. HAMI 3379 inhibited release of the cytokines IL-1b, interferon-c (IFN-c), and tumor necrosis factor-a (TNF-a) into the serum and cerebrospinal fluid, microglial activation and neutrophil accumulation, inhibited astrocyte proliferation and reduced serum IL-4 [28].

Oleoylethanolamie

30 mg/kg

MCAO. For    120 min, 24 hr reperfusion

Behavioural parameters Morris water maze test, Electrophysiological recordings, Biochemical parameters-Immunohistochemisty and cell counting, Western blot

OEA markedly increased the expressions of brain-derived neurotrophic factor (BDNF) and peroxisome proliferator-activated receptors α(PPAR α). Chronic OEA treatment can exert functional recovery of cognitive impairments and neuroprotective effects   via triggering of neurogenesis in the hippocampus [29].

scopolamine and mecamylamine

0.1mg/kg, 0.5mg/kg

BCCAO for 45 min, reperfusion for 8 days.

Behavioural parameters Morris water maze, Biochemical parameters-Lactate dehydrogenase activity assay, Determination of caspase activity, acetylcholinesterase (AChE) activity, Determination of choline acetyltransferase activity (ChAT)

Scopolamine and mecamylamine alters memory functions following GCI/R injury substantiating the combined functional importance of both muscarinic and nicotinic receptor modulation in memory dysfunction [30].

Nitric Oxide, N-nitro-L-arginine methyl ester (L-NAME),

 

BCCAO for 10 min, 24 h reperfusion

Rat brain hippocampus cell dissociation, Flow cytometric analysis, infarct volume measurement, Nitric Oxide detection in vivo

Increased NO concentration, CBF significantly. Reduced infarct size and down regulated the cell death and reduced the brain injuries [31].

 

 

 

 

3,5,6,7,8,3’,4’-Heptamethoxy flavones

25 & 50 mg/kg

BCCAO for 12min reperfusion 72 hr

Y-maze test, Immunofluorescence for confocal microscopy

Protected against ischemia-induced memory dysfunction, rescued neuronal cell death in the CA1 cell layer, increased the production of BDNF, stimulated the autophosphorylation of CaMK II and suppressed microglial activation in the hippocampus [32].

Rosiglitazone

3 mg/kg

BCCAO  reperfusion 24 or 72 hr

Measurement of reduced glutathione (GSH) in brain tissue, Measurement of malondialdehyde (MDA) in brain tissue, Measurement of myeloperoxidase (MPO),

PPAR-γ agonist, demonstrated preservation of cell viability of CA1 hippocampal region and attenuation of brain edema. They also showed elevated levels of GSH and low levels of the other parameters In vitro, rosiglitazone dose-dependently inhibited ROS generation by neutrophils [33].

 

Puerarin

2.62, 7.86

and 23.59 mg/kg

MCAO for 2 h

Cell viability, Oxygen glucose deprivation/reperfusion assay, Flow cytometry, Immunohistochemistry, Western blot analysis, Nissl stain

Puerarin treatment significantly improved the phosphorylation level of AKT in dose-dependent, reduced the infarct volume, The number of Nissl body, cleaved caspase-3 and GFAP positive cells increased [18].

NOW YOU CAN ALSO PUBLISH YOUR ARTICLE ONLINE.

SUBMIT YOUR ARTICLE/PROJECT AT editor-in-chief@pharmatutor.org

Subscribe to Pharmatutor Alerts by Email

FIND OUT MORE ARTICLES AT OUR DATABASE


Pages

FIND MORE ARTICLES