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Page 1: Neuroprotection after stroke · 2006. 1. 6. · Neuroprotection after stroke Stroke is major cause of morbidity and death in the elderly population. Al-though a small proportion of

CMAJ • January 17, 2006 • 174(2) | 152

News

Neuroprotection

after stroke

Stroke is major cause of morbidity anddeath in the elderly population. Al-though a small proportion of patientswho experience stroke arrive at hospitalearly enough for reperfusion therapy,for most patients the treatment optionsare limited. Neuronal death as a resultof inflammation and apoptosis contin-ues after the initial ischemic insult.New research reveals a potential targetthat might help to limit neuronal death.

A molecule called NF-κB is knownto have antiapoptotic effects in non-neuronal cells. Oliver Herrmann andcolleagues targeted an enzyme calledIKK2 that regulates the activation of theNF-κB protein. The scientists created 2strains of mice: one that lacked IKK2 inneurons and another in which IKK2was always turned on in the same cells.They found that, after induced cerebralischemia, mice lacking IKK2 had re-duced infarct size compared with micein which IKK2 was activated (NatureMed 2005; doi:10.1038/nm1323).

The results suggest that pharmaco-logic inhibition of IKK2 might be suc-cessful in the treatment of stroke. Sev-eral IKK2 inhibitors already exist.Herrmann and colleagues found thatadministration of a known IKK2 in-hibitor after cerebral ischemia in micereduced the volume of cell death by60%. This effect worked for up to 4.5hours after the stroke, which may bodewell for human patients who requiretime to reach a hospital.

have received attention over the years aspotential antiseptics, spasmolytics, di-uretics and antidepressants.

To determine its antiviral properties,the authors extracted p27SJ from cul-tured cells of the St. John’s Wort plantand found that, in human cells infectedwith HIV-1, the extract suppressed thetranscription of the viral genome. Thescientists determined that p27SJ is ableto do this by interacting with 2 keyproteins involved in HIV replication.When injected into microglial cellsalong with HIV-1, p27SJ reduced viralreplication by almost 50% (Gene Ther2005; doi:10.1038/sj.gt.3302649).

St. John’s Wort is widely available asan herbal supplement. Whether com-mercially available preparations con-tain p27SJ is unclear, and their use as al-ternative therapy for HIV infection isnot recommended. Rather, the find-ings should be interpreted as hypothe-sis generating. — Compiled by DavidSecko, Vancouver

HIV stalled

by St. John’s Wort

St. John’s Wort, a widely used herbalremedy for depression, has been re-cently shown to contain a componentthat inhibits HIV replication. Althoughthe findings are preliminary and theprotein, named p27SJ, is far from beingrecommended as a treatment for HIVinfection, the findings suggest the pos-sibility of alternative therapeutic strate-gies for HIV infection.

Nune Darbinian-Sarkissian and col-leagues recently discovered p27SJ whilelooking at the effects of plant extractsfrom St. John’s Wort on the behaviourof brain cells in culture. Such extracts

Bench to Bedside

DOI:10.1503/cmaj.051539

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