Re: Pain/Brain/Modulators

[Guest guest]

Interesting that I can't handle mincocyline, but Benicar works

great, whereas two of my friends found that Benicar did nothing for

them, but minocycline works great. If I had the patience, perhaps I

could distinguish from the info below, what those different

responses mean and why the exist. I can also say that those two

people are on the opposite end of the metabolism scale from me. Very

quick metabolisms, can eat massive amounts of food, one is actually

hyperthyroid, where I'm hypo.

penny

> Since I used Ibuprofen (and my drug choices) becuase of addirional

> mechanism besides antibacterial... here's a few more abstracts

>

> Good description of microglia in the first one.

>

> >

> > all interesting abstracts on Mino at this addy:

> > http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?SUBMIT=y

> >

> > all interesting abstracts on ibuprofen at this addy

> > http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?SUBMIT=y

> >

> > Arch Pharm Res. 2004 Mar;27(3):314-8. Related Articles, Links

> >

> >

> > Inhibitory action of minocycline on lipopolysaccharide-induced

> > release of nitric oxide and prostaglandin E2 in BV2 microglial

> cells.

> >

> > Kim SS, Kong PJ, Kim BS, Sheen DH, Nam SY, Chun W.

> >

> > Department of Pharmacology, College of Medicine, Kangwon National

> > University, Chunchon 200-701, Korea.

> >

> > Microglia are the major inflammatory cells in the central nervous

> > system and become activated in response to brain injuries such as

> > ischemia, trauma, and neurodegenerative diseases including

> > Alzheimer's disease (AD). Moreover, activated microglia are known

> to

> > release a variety of proinflammatory cytokines and oxidants such

> as

> > nitric oxide (NO). Minocycline is a semisynthetic second-

> generation

> > tetracycline that exerts anti-inflammatory effects that are

> > completely distinct form its antimicrobial action. In this study,

> the

> > inhibitory effects of minocycline on NO and prostaglandin E2

> (PGE2)

> > release was examined in lipopolysaccharides (LPS)-challenged BV2

> > murine microglial cells. Further, effects of minocycline on

> inducible

> > nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2)

> expression

> > levels were also determined. The results showed that minocycline

> > significantly inhibited NO and PGE2 production and iNOS and COX-2

> > expression in BV2 microglial cells. These findings suggest that

> > minocycline should be evaluated as potential therapeutic agent

for

> > various pathological conditions due to the excessive activation

of

> > microglia.

> >

> > PMID: 15089037 [PubMed - indexed for MEDLINE

>

> __________________________________________________________________

> >

> >

> > : Neurobiol Dis. 2004 Jun;16(1):190-201. Related Articles, Links

> >

> >

> > Minocycline reduces the lipopolysaccharide-induced inflammatory

> > reaction, peroxynitrite-mediated nitration of proteins,

disruption

> of

> > the blood-brain barrier, and damage in the nigral dopaminergic

> system.

> >

> > Tomas-Camardiel M, Rite I, Herrera AJ, de Pablos RM, Cano J,

> Machado

> > A, Venero JL.

> >

> > Departamento de Bioquimica, Bromatologia, Toxicologia y Medicina

> > Legal Facultad de Farmacia, Universidad de Sevilla, E-41012-

> Seville,

> > Spain.

> >

> > We have evaluated the potential neuroprotectant activity of

> > minocycline in an animal model of Parkinson's disease induced by

> > intranigral injection of lipopolysaccharide. Minocycline

treatment

> > was very effective in protecting number of nigral dopaminergic

> > neurons and loss of reactive astrocytes at 7 days postlesion.

> > Evaluation of microglia revealed that minocycline treatment

highly

> > prevented the lipopolysaccharide-induced activation of reactive

> > microglia as visualized by OX-42 and OX-6 immunohistochemistry.

> Short-

> > term RT-PCR analysis demonstrated that minocycline partially

> > prevented the lipopolysaccharide-induced increases of mRNA levels

> for

> > interleukin-1alpha and tumor necrosis factor-alpha. In addition,

> > lipopolysaccharide highly induced protein nitration as seen by 3-

> > nitrotyrosine immunoreactivity in the ventral mesencephalon.

> > Minocycline treatment strongly diminished the extent of 3-

> > nitrotyrosine immunoreactivity. We also found a direct

correlation

> > between location of IgG immunoreactivity-a marker of blood-brain

> > barrier disruption-and neurodegenerative processes including

death

> of

> > nigral dopaminergic cells and reactive astrocytes. There was also

> a

> > precise spatial correlation between disruption of blood-brain

> barrier

> > and 3-nitrotyrosine immunoreactivity. We discuss potential

> > involvement of lipopolysaccharide-induced formation of

> peroxynitrites

> > and cytokines in the pathological events in substantia nigra in

> > response to inflammation. If inflammation is proved to be

involved

> in

> > the ethiopathology of Parkinson's disease, our data support the

> use

> > of minocycline in parkinsonian patients.

> >

> > PMID: 15207276 [PubMed - indexed for MEDLINE]

> >

> >

> >

> > ____________________________________________________________

> > J Neurovirol. 2004 Oct;10(5):284-92. Related Articles, Links

> >

> >

> > A novel action of minocycline: inhibition of human

> immunodeficiency

> > virus type 1 infection in microglia.

> >

> > Si Q, Cosenza M, Kim MO, Zhao ML, Brownlee M, Goldstein H, Lee S.

> >

> > Department of Pathology, Albert Einstein College of Medicine,

> Bronx,

> > New York 10461, USA.

> >

> > Human immunodeficiency virus type 1 (HIV-1) infection of the

brain

> > produces a characteristic disease called acquired

immunodeficiency

> > syndrome (AIDS) dementia in which productive infection and

> > inflammatory activation of microglia and macrophages play a

> central

> > role. In this report, the authors demonstrate that minocycline

> (MC),

> > a second-generation tetracycline with proven safety and

> penetration

> > to the central nervous system, potently inhibited viral

production

> > from microglia. Inhibition of viral release was sustained through

> the

> > entire course of infection and even when the drug exposure was

> > limited to the first day of infection.

> >

> > Minocycline was effective even at low viral doses, and against

R5-

> > and X4R5-HIV, as well as in single-cycle reporter virus assays.

> >

> > Electrophoretic mobility shift analysis showed that minocycline

> > inhibited nuclear factor (NF)-kappaB activation in microglia.

> >

> > HIV-1 long terminal repeat (LTR)-promoter activity in U38 cells

> was

> > also inhibited. These results, combined with recently

demonstrated

> in

> > vivo anti-inflammatory effects of MC on microglia, suggest a

> > potential utility for MC as an effective adjunct therapy for AIDS

> > dementia.

> >

> > PMID: 15385251 [PubMed - in process]