Friday Hope: Berberine: Inhibiting Activation of Fibrocytes

Berberine also inhibits inflammation, making it a potentially very important player in dealing with the Spike Protein.

It is well known that Pulmonary Fibrosis is a complication of COVID and Spike Protein exposure.

Here, we found that S1 injection in mice transgenic for human angiotensin converting enzyme 2 (ACE2) induced early loss of lung endothelial thromboresistance at 3 days, as revealed by thrombomodulin loss and von Willebrand factor (vWF) increase. In parallel, vascular and epithelial C3 deposits and enhanced C3a receptor (C3aR) expression were observed. These changes preceded diffuse alveolar damage and lung vascular fibrin(ogen)/platelets aggregates at 7 days, as well as inflammatory cell recruitment and fibrosis.

SARS-CoV-2 spike protein induces lung endothelial cell dysfunction and thrombo-inflammation depending on the C3a/C3a receptor signalling
https://www.nature.com/articles/s41598-023-38382-5

Per my most recent post, I believe the Spike Protein is jnducing systemic fibrosis via a mechanism parallel to radiation.

Indeed, is evidence that the fibrosis caused by the Spike Protein is not limited to the lungs.

Our data demonstrated that the Spike protein could induce long-term transcriptional suppression of mitochondria metabolic genes and cause cardiac fibrosis and myocardial contractile impairment, providing mechanistic insights to PACS-related cardiomyopathy.

The SARS-CoV-2 Spike protein induces long-term transcriptional perturbations of mitochondrial metabolic genes, causes cardiac fibrosis, and reduces myocardial contractile in obese mice
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9844011/

Therefore, it is important that we find therapeutics to deal with this condition. I have discovered that Berberine is a very beneficial compound in not only treating, but perhaps preventing fibrosis in that it inhibits the activation of fibroblasts.

The experimental results show that berberine can regulate cell proliferation, metabolism, mainly through tumor necrosis factor-α (TNF-α), interleukin 6 (IL-6), activator of transcription (STAT3) and chemokine ligand 2 (CCL2) and survival, thereby exerting a therapeutic effect on COVID-19 pneumonia pulmonary fibrosis.

Also, I believe Berberine may also prove useful in inhibiting the potential systemic fibrosis caused by the Spike Protein.

Studies have indicated that, in the model of pulmonary fibrosis berberine inhibition of rapamycin target protein mTOR activated to enhance cell autophagy and inhibits fibrosis.

Research on the mechanism of berberine in the treatment of COVID-19 pneumonia pulmonary fibrosis using network pharmacology and molecular docking
https://www.sciencedirect.com/science/article/pii/S2667031322000380#sec0025

I will continue to pursue treatments and preventative measures for the observed Spike Protein induced fibrosis. As with all medicines and supplements, please consult your Primary Care Provide before use, as this post is not medical advice, but a work of medical research.

I wish all a peaceful, restful and joyous weekend.