Hi! I am not aware of any significant differences of the antioxidant defense or the role of oxidative stress in the pathophysiology of ischemic damage between male and female patients. Essentially, if you work with stroke animal models (e.g. rats) the molecular events and the gross pathology following hypoxia/ischaemia will not differ massively  between both sexes. The potential role of estrogens should not be over-estimated (my personal opinion). To my best knowledge, clinical attempts to use antioxidants to limit stroke damage were mostly disappointing in both female and male patients.

As far as i know, there is no discernible difference. often in studies they will use one sex over another (in rats, typically female....just easier to handle). As Just mentioned, there is an influence of estrogens (and related hormones), but not a significant one to justify using it as a  pharmacological target.

I have no idea, why should there be differences in neuroprotection by antioxidant between male and female. If you have any highly convincing literature's, please do share with us. So that we can discuss the problem.

Side effects arising from estrogen exposure post menopause, we are trying to use alternative method to prevent stroke damage and post stroke recovery.  According to one of the paper which is on chronic stress  "GINKGO BILOBA EXTRACT EGb 761 ATTENUATES HIPPOCAMPAL NEURONAL LOSS AND COGNITIVE DYSFUNCTION RESULTING FROM CHRONIC RESTRAINT STRESS IN OVARIECTOMIZED RATS"  suggests that antioxidant attenuates CA3 hippocampal damage and independent of ER pathway. 

Hi Jatin, this study was female subject (344 Fisher female rat in three groups) and there is no male subject for the comparison. Therefore, your statements of deference's between male and female neuroprotection by anti-oxidant is not correct. If you have the print manuscript (pdf), please share with us to understand the molecular mechanism of how GINKGO could do the neuroprotection.   

We studied the effect of quercetin ( strong antioxidant ) on gerbil of both sex after ischemic injury and did not see any differences in neuroprotection. Please, if you know some literature, share with us

Quercetin is known to upregulate HO-1/Nrf2 pathway in male mice, but in females role of antioxidants is still elusive. We recently published a paper on EGb 761 in males that it promotes neurogenesis via HO-1/Wnt pathway in males. Did quercetin  protect OVX females following stroke?

This one is very peculiar, as it points that the universally prescribed Corticosteroid for Brain edema: Dexametasone, may not actually be an evidence based first choice, just the enormous size of the sample for conducting a comparative study of Dexametasone vs 6-methyl-Prednisolone at equipotentedoses precludes considering this, besides that no pharmaceutical company would invest in a product no longer having a patent protection, but the content of this article is what it is:

Neurosurgery. 1980 Feb;6(2):149-54.

Ischemic cerebral edema in primates: effects of acetazolamide, phenytoin,

sorbitol, dexamethasone, and methylprednisolone on brain water and electrolytes.

Bremer AM, Yamada K, West CR.

Brain edema was induced in primates (Macaca mulatta) after regional cerebral

ischemia produced by selective embolization of the internal carotid artery

bifurcation. Details of the alterations in the distribution of water and

electrolytes in the brain during the evolution of ischemic cerebral edema have

been described elsewhere. The effects of five theoretically useful

pharmacological agents were studied. Acetazolamide failed to improve ischemic

edema and, rather, increased mortality. Phenytoin definitely prevented both edema

and infarction in only the cerebral cortex. Sorbitol was effective to induce

dehydration of the affected cortex and the normal brain tissue, with obvious

reduction of the brain bulk. High dose steroids showed an ability to modify edema

in the cortex, putamen, and white matter. However, animals treated with

methylprednisolone rather than dexamethasone showed a better neurological

recovery and smaller infarcts.

PMID: 6767997  [PubMed - indexed for MEDLINE]

(Conflict of interest: I'm a former employee of the Upjohn company, Spain, producers of 6-Methyl-Prednisolone)

long before it has been stablished that antioxidant confer protective role both in female an\d male. plz can u send any papers that support your question.

Estrogen upregulates all the necessary protiens in the body including antioxidants considering side effects are harmful as well in estrogen replacement therapy. The mechanism by which our compound works is solely but antioxidant pathway in male mice and we have published several papers. But when same compounds was used in ovaryectomized  female mice neuroprotection was independent of antioxidant pathway. Together my preliminary data suggested that female neuroprotection is independent of antioxidant pathway. My compound also induced neurogenesis similar to that of estrogen pathway but with a different mechanism. Please share papers related to natural compounds and female neuroprotection.

Around 1976, some proposed the IV dosing of Theophiline for those having suffered a very recent Stroke, Theophyllin is an AdenylCyclase inhibitor, and by reducing the intracellular levels of CyclicAMP, it reduces overall Cell activity, thus reducing consequences of any Stressor acting on the Brain Cells, the administration of very high doses of Dxamethasone was also proposed for traumatic head injuries, sorry, I don't remember exactly the range, perhaps above 40 mg Dexa, but what should also be remembered is that any IV dose of 6-Methyl-Prednisolone above 20-40 mg should be injected in at least 20 min, to reduce the risk of potentially lethal Cardiac Arrythmia linked to fast IV Corticosteroid Bolus. Thanks.

Salud †