NAC (N-Acetyl-L-Cysteine) also lowers MMP-9s as well as some other nasty things.

I take 600 mg a day (Vitamin Shoppe $17.17 for 100 capsules)

jackD

1: J Clin Endocrinol Metab. 2003 Apr;88(4):1723-9.

N-Acetyl-cysteine inhibits phospholipid metabolism, proinflammatory cytokine
release, protease activity, and nuclear factor-kappaB deoxyribonucleic
acid-binding activity in human fetal membranes in vitro.

Lappas M, Permezel M, Rice GE.

Department of Obstetrics and Gynecology, University of Melbourne, and Mercy
Perinatal Research Center, Mercy Hospital for Women, East Melbourne, 3002
Victoria, Australia. mlappas@unimelb.edu.au

The production of reactive oxygen species (ROS), prostaglandins (PGs),
proinflammatory cytokines, and proteases has been implicated in the pathogenesis
of term and preterm labor. The nuclear factor-kappaB (NF-kappaB) transcription
pathway is activated by ROS and is a key regulator of PGs, proinflammatory
cytokine release, and protease activity. N-Acetyl-cysteine (NAC) is an
antioxidant that through its ability to scavenger ROS suppresses NF-kappaB
DNA-binding activity and resultant gene expression. The aim of this study was to
elucidate the effect of NAC on NF-kappaB DNA-binding activity, phospholipid
metabolism, cytokine release, and protease activity from human fetal membranes.
Human amnion and choriodecidua (n = 9 separate placentas) were treated with 0
(control), 5, 10, or 15 mM NAC in the presence of 10 micro g/ml
lipopolysaccharide. After 6-h incubation, the tissues were collected, NF-kappaB
DNA binding activity was assessed by gel shift binding assays, and matrix
metalloproteinase-9 and urokinase-type plasminogen activator activity were
determined by zymography. The incubation medium was collected and assayed for
type II phospholipase A(2) tissue content, IL-6, IL-8, TNFalpha, and
8-isoprostane release by ELISA. The release of PGF(2alpha) was measured by RIA.
Treatment of fetal membranes with NAC significantly suppressed
lipopolysaccharide-stimulated type II phospholipase A(2) release and content;
PGF(2alpha), IL-6, IL-8, TNFalpha, and 8-isoprostane release; and matrix
metalloproteinase-9 and urokinase-type plasminogen activator enzyme activity and
suppressed NF-kappaB DNA-binding activity (by ANOVA, P < 0.05). The data
presented in this study demonstrate that NAC inhibits an NF-kappaB-activated
pathway and subsequent phospholipid metabolism, proinflammatory cytokine
release, and protease activity in human fetal membranes.

PMID: 12679464 [PubMed - indexed for MEDLINE]
1: Biofactors. 1999;10(2-3):187-93.

N-Acetyl-cysteine inhibition of encephalomyelitis Theiler's virus-induced nitric
oxide and tumour necrosis factor-alpha production by murine astrocyte cultures.

Molina-Holgado F, Hernanz A, De la Fuente M, Guaza C.

Neural Plasticity Unit, Instituto Cajal, CSIC, Madrid, Spain.

The pathological mechanisms that cause central nervous system (CNS) dysfunction
in most neurological diseases are not well established. Theiler's murine
encephalomyelitis virus (TMEV) is known to interact with cells of the CNS and
its intracerebral inoculation to susceptible mice strains causes neurological
disorders resembling multiple sclerosis (MS). In this study, we reported that
primary astrocyte cultures from SJL/J susceptible mice when infected with TMEV
released important amounts of nitrites (NO2-) to the culture medium, as measured
in the supernatants 24 hours after infection. In addition, we observed an
increment in the production of tumour necrosis factor alpha (TNF-alpha) by
susceptible SJL/J strain derived astrocytes infected with TMEV. The treatment
with the thiolic antioxidant N-acetyl-cysteine partially suppressed the
virus-stimulated production of nitric oxide and TNF-alpha, in a dose response
fashion. These results indicate that during viral infection astrocytes are an
important cellular source of nitric oxide and TNF-alpha, substances which play
important roles during CNS inflammatory events. The effects of the antioxidant
N-acetyl-cysteine, modulating the production of the above compounds by
TMEV-infected astrocytes may be a significant factor in preventing CNS
demyelination.
PMID: 10609881 [PubMed - indexed for MEDLINE]