HMG-CoA reductase

And that is basically what's going on with black cumin seed and turmeric.

Black cumin has an ingredient in it called phymoquinone, which is an HMG-CoA reductase inhibitor.

That is the same mechanism of action as the statins.

So black cumin has like a little statin in it.

And so there is a sterile sensor in the liver called SREBP2, sterile regulatory element binding protein 2.

And it dictates the transcription of HMGCR, which is cholesterol synthesis.

LDL receptor, which is the claw grabber that pulls in the LDL particle from the periphery.

And then also it dictates the transcription of PCSK9.

No, no, no.

There was 11 with HMGCR.

That's the statin-associated HMG co-reductase marker.

There were three with signal recognition particle disease, two seronegative, three with dermatomyositis, one TIF gamma, one NXP2.

The metabolic side of things, yes.

When evaluating the anti-hyperlipidemics, specifically the statins or HMG-CoA reductase inhibitors, the SAR requires an incredibly specific geometry.

Nevastatin and lavastatin are the lead compounds, and the textbook data shows that the ethylene bridge connecting the lactone ring to the bicyclic ring is absolutely critical.

It is non-negotiable.

And for our listeners, I'm not gonna get too technical, but I'm gonna share this, um, for Jim.

Um, I shared, I talked through the HMG-CoA reductase pathway, right? And basically for our listeners, what that is, is for those statin drugs to work, they have to use CoQ10.

Um, CoQ10, we've all heard about CoQ10, ubiquinol, or ubiquinone, um, ubiquitous hormone.

Um, it, they need it.

The T cells require a great deal of lipogenesis, including cholesterol.

So by increasing the expression of the genes, for example, coding HMG-CoA reductase, and the LDL-R, the receptor, that's going to enhance de novo cholesterologenesis, but also entire preno lipid synthesis.

And those other preno lipids are all part of an anabolic activity.

For example, dolycopyrophosphate, which is not part of the cholesterol arm of the preno lipid synthesis starting from HMG-CoA reductase, that's necessary for the production of all the glycoproteins.

So that's happening de novo in the cell, in the T cell.

You also have uptake of cholesterol from LDL-C because more LDL-R is on the surface.

Now there's some oxysterol that's generated in the activated T cell.

And that oxysterol moving through a protein called SULT2B1 allows for the production of sulfated oxysterols.