It appears we are dealing with PLA2-IIA which is upregulated by not only TNF alpha, but IL 1 B as well.
The body tries to downregulate PLA2-IIA via making a lot of arachidonic acid which is an Omega 6 fatty acid.
"The arachidonic acid pathway constitutes one of the main mechanisms for
the production of ***pain*** and inflammation,
as well as controlling homeostatic function."
Why is this important? (NMDA are glutamate receptors)
"Since exogenous sPLA2-IIA has been shown to
cause neuronal injury,
understanding the mechanism(s) and physiological consequences of sPLA2-IIA upregulation in AD (Alzheimer's Disease) brain may facilitate the development of novel therapeutic strategies to inhibit the inflammatory responses and to retard the progression of the disease."
"Inhibition of secretory PLA2-IIA (i)
reduced the generation of ROS after glutamate treatment,
(ii) reduced the ROS production in peripheral mitochondria in glutamate-treated neurons, consistent with the fact that
calcium entry through glutamate (NMDA) receptors has a privileged access to peripheral mitochondria, and
(iii) did not reduce the generation of ROS after buffer treatment.
In conclusion, activation of NMDA receptors induces ROS, which is critical for neuronal death,
***due to*** secretory PLA2-IIA associated with peripheral mitochondria.
If I were you, I'd get on OmegaBrite asap and very high doses spaced out.
Gotta reduce the brain inflammation!
"In addition to apocynin, a known NADPH oxidase inhibitor, botanical antioxidants, such as
resveratrol (my note...wanna talk about transducin?) and *epigallocatechin gallate*,
also inhibited IL-1β-induced sPLA2-IIA mRNA expression. These compounds also suppressed IL-1β-induced ERK1/2 activation and translocation of the NADPH oxidase subunit p67 phox from cytosol to membrane fraction."
Guess what epigallocatechin gallate is in...
Green tea extract!
Wanna talk about the "magic five" again?
I think it is gonna take a LOT to work...spaced out.
AND...we may have to deal with NH3 via ACZ zeolite (FDA okay'd) to bind NH3 (ammonia) as the proteins are broken down when Bb AND the cells it was infecting are destroyed.
"Glucocorticoids indirectly inhibit the activity of phospholipase A2, an enzyme that plays an essential role in the synthesis of prostaglandins and leukotrienes; its inhibition by lipocortin-1 underlies part of the anti-inflammatory effects..."
But glucocortiods (steroids) are bad news in lyme. They look to help Bb out. Bb maybe counting on that response.
What OTHER MAJOR antiflammatory is really what is needed and is "missing"?
If you didn't say Magnesium...you get an "F" for today's lesson.
Increase GTP (Guanosine-5'-triphosphate) and close the Na-Ca channel. THEN Mg can cause GTP-> cGMP (tri to mono) + PPi (= pyrophosphate)
"Magnesium for Autoimmune" by Dr. Valletta.
He used *MgPyrophosphate* AND sub(lingual) B6 to cure RA, ulcerative colitis and invasive bowel cancer in MONTHS.
(This process was "jumpstarted" with IV dosages.)
Phospholipase A2 is a small lipolytic enzyme that
releases fatty acids from the second carbon group of glycerol.
It is involved in a number of physiologically important cellular processes, such as the
liberation of arachidonic acid
from membrane phospholipids. It plays a pivotal role in the biosynthesis of prostaglandin and other mediators of inflammation.
PLA2 has four to seven disulphide bonds and binds a *calcium ion that is essential for activity*.
Within the active enzyme, the alpha amino group is involved in a conserved hydrogen-bonding network linking the N-terminal region to the active site. The side chains of two conserved residues, His and Asp, participate in the catalytic network.
Many PLA2's are widely distributed in snakes,
lizards,
bees and mammals.
In mammals there are at least four forms: pancreatic, membrane-associated as well as two less well characterised forms.
The venom of most snakes contains multiple forms of PLA2.
Some of them are presynaptic neurotoxins which inhibit neuromuscular transmission by
Is Bb's toxin preventing the release of acetylcholine?
Looks that way.
Why would it be important acetylcholine NOT be released?
It opens Na channels.
Bb NEEDS sodium...for it's Na-ATPase and NaCl for motility.
Bb also INHIBITS calcium (PKC inhibitor)...
So what do we do in response to Bb which looks to NOT want, but DOES in fact need, Na or Ca?
We send those electrolytes into the cells.
Getting inflammation down (IDEALLY with IV MgCL) looks to make ALL other forms of treatments more effective to destroy Bb.
It CAN be done.
We gotta block TNF alpha, IL1 B, and inhibit PLA2-IIA.
Counter them.
Posted by seekhelp (Member # 15067) on :
Can you PLEASE let us know if anyone has been doing the Magic 5 and reporting favorable results? I REALLY need to know.
Posted by polar blast (Member # 9142) on :
marnie why does bb become vulnerable to attack from the
immune system when taking anyibiotics with green
tea?
why do i always feel better if i take mag?
Posted by Dawn in VA (Member # 9693) on :