Billions wasted on statins and the associated damage they've done when it should have been CoQ10, Serrapeptase, aged garlic extract, Magnesium

You know, the stuff that will prevent diabetes, not egg it on.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10047379/ 

SRP inhibits inflammation and oxidative stress through the endothelium MCP-1. We concluded that SRP has the ability to modulate vascular inflammation. Further studies will be required to explore the detailed mechanisms of the cardio-protective effects produced by SRP.Mar 8, 2023

5. Conclusions

In conclusion, our work demonstrates that SRP can attenuate the elevated inflammatory biomarkers (MCP-1, IL-2, IL-4, IL-6, and TNF-α), the production of MDA, ROS intensity, CATx, and GSH impact in the setting of LPS-induced vascular inflammation. SRP inhibits inflammation and oxidative stress through the endothelium MCP-1. We concluded that SRP has the ability to modulate vascular inflammation. Further studies will be required to explore the detailed mechanisms of the cardio-protective effects produced by SRP. These results suggest that serratiopeptidase may be a therapeutic agent for vascular inflammation in cardiovascular diseases.

https://pubmed.ncbi.nlm.nih.gov/36975512/ 

Serratiopeptidase Attenuates Lipopolysaccharide-Induced Vascular Inflammation by Inhibiting the Expression of Monocyte Chemoattractant Protein-1 

Abstract

Lipopolysaccharide (LPS) has potent pro-inflammatory properties and acts on many cell types including vascular endothelial cells. The secretion of the cytokines MCP-1 (CCL2), interleukins, and the elevation of oxidative stress by LPS-activated vascular endothelial cells contribute substantially to the pathogenesis of vascular inflammation. 

However, the mechanism involving LPS-induced MCP-1, interleukins, and oxidative stress together is not well demonstrated. Serratiopeptidase (SRP) has been widely used for its anti-inflammatory effects. 

In this research study, our intention is to establish a potential drug candidate for vascular inflammation in cardiovascular disorder conditions. We used BALB/c mice because this is the most successful model of vascular inflammation, suggested and validated by previous research findings. 

Our present investigation examined the involvement of SRP in vascular inflammation caused by lipopolysaccharides (LPSs) in a BALB/c mice model. We analyzed the inflammation and changes in the aorta by H&E staining. SOD, MDA, and GPx levels were determined as per the instructions of the kit protocols. 

ELISA was used to measure the levels of interleukins, whereas immunohistochemistry was carried out for the evaluation of MCP-1 expression. SRP treatment significantly suppressed vascular inflammation in BALB/c mice. 

Mechanistic studies demonstrated that SRP significantly inhibited the LPS-induced production of proinflammatory cytokines such as IL-2, IL-1, IL-6, and TNF-α in aortic tissue. 

Furthermore, it also inhibited LPS-induced oxidative stress in the aortas of mice, whereas the expression and activity of monocyte chemoattractant protein-1 (MCP-1) decreased after SRP treatment. In conclusion, SRP has the ability to reduce LPS-induced vascular inflammation and damage by modulating MCP-1.

Keywords: lipopolysaccharides; monocyte chemoattractant protein-1; oxidative stress; serratiopeptidase; vascular inflammation; vascular smooth muscle cells.