Fibrosis, also known as fibrotic scarring, is a pathological wound healing in which connective tissue replaces normal parenchymal tissue to the extent that it goes unchecked, leading to considerable tissue remodelling and the formation of permanent scar tissue. Repeated injuries, chronic inflammation and repair are susceptible to fibrosis where an accidental excessive accumulation of extracellular matrix components, such as the collagen is produced by fibroblasts, leading to the formation of a permanent fibrotic scar.
In response to injury, this is called scarring. Physiologically, fibrosis acts to deposit connective tissue, which can interfere with or totally inhibit the normal architecture and function of the underlying organ or tissue. Fibrosis can be used to describe the pathological state of excess deposition of fibrous tissue, as well as the process of connective tissue deposition in healing. Defined by the pathological accumulation of extracellular matrix (ECM) proteins, fibrosis results in scarring and thickening of the affected tissue, it is in essence an exaggerated wound healing response which can interfere with normal organ function.
FIBROHIB™ is a broad-based nutraceutical formula containing herbal extracts and other nutrients. FIBROHIB™ aims to reduce TGFb, Matrix metalloproteinases (MMP’s) and other pathways which drive inflammatory, immune disorders, necrosis, scarring & fibrogenesis. The formula contains a number of natural ingredients shown in studies to help inhibit the processes underlying fibrogenesis such as Astragalus, Silimarin, Quercetin, Salvia, Ginseng, Ginger, Berberine and EGCG. By also combining with Vitamin E, Omega 3 DHA , NICLOSTEM™ and Serrapeptase, these can help reduce inflammatory processes and may even help break down existing scarring and necrosis.
TGF-ß is one of the most important mediators involved in fibrogenesis; 3 isoforms are expressed in mammalians, known as TGF-ß1, TGF-ß2, and TGF-ß3, encoded by different genes . TGF-ß acts as a pleiotropic signal of different effects; the interaction with its specific receptor may induce signals of migration/differentiation and may stimulate integrin expression, thus promoting adhesion process, (ii) regulates macrophages function stimulating the release of pro-fibrotic mediators , depresses T cell proliferation through IL-2 inhibition, promotes the shutdown of the inflammatory response by inhibiting pro-inflammatory cytokines and chemokines expression, induces fibroblasts differentiation into myofibroblasts. [source]
A paramount role in the reparative processes is attributed to TGFß that induces fibroblasts differentiation into myofibroblasts and stimulates the release of type I collagen and connective tissue growth factor (CTGF); moreover, TGFß decreases metalloproteinases levels with consequent collagen accumulation. Therefore, the unbalanced activation of TGFß may exacerbate fibrotic process worsening the quality of the scar; in addition, TGFß over-activation might be considered as a negative predictor factor for heart failure. Decreased TGFb and LRP1 signals impairs myofibroblast differentiation which decreases fibrosis. [source]
FIBROHIB™ is a broad-based nutraceutical formula containing herbal extracts and other nutrients. FIBROHIB™ aims to reduce Matrix metalloproteinases (MMP’s) and other pathways which drive inflammatory, immune disorders, necrosis & fibrogenesis. FIBROHIB™ may best be supported with Vitamin E, Omega 3 DHA , NICLOSTEM™ and Serrapeptase, these can help reduce inflammatory processes and may even help break down existing scarring and necrosis.
Take 2-4 capsules 3x a day, 30 mins after food in the morning / evening or as directed by a health professional. Do not use soon after surgery as it may impede healing.
Panax Ginseng extract had an anti-fibrosis effect via the regulation of the TGF-ß1/Smad signaling pathway in the CCl4-induced liver fibrosis model. The major target was the inhibition of the expression of TGF-ß1, Smad2, and Smad3.
Compound Astragalus and Salvia miltiorrhiza Extract exerts anti-fibrosis by mediating TGF-ß/Smad signaling in myofibroblasts.
Epigallocatechin gallate (EGCG) attenuates fibrosis, oxidative stress, and inflammation in non-alcoholic fatty liver disease rat model through TGF/SMAD, PI3 K/Akt/FoxO1, and NF-kappa B pathways. Treatment with EGCG improved hepatic histology (decreased number of fatty score, necrosis, and inflammatory foci), reduced liver injury (from ~0.5 to ~0.3 of ALT/AST ratio), attenuated hepatic changes including fibrosis (reduction in Sirius Red and synaptophysin-positive stain) with down-regulation in the expressions of key pathological oxidative (e.g. nitrotyrosine formation) and pro-inflammatory markers (e.g. iNOS, COX-2, and TNF-a). EGCG treatment also counteracted the activity of TGF/SMAD, PI3 K/Akt/FoxO1, and NF-kB pathways.
Silimarin & Ginger
Galectin-8 (Gal-8) is downregulated in liver fibrosis. Reduced Gal-8 expression correlates with inflammation and metastasis. Gal-8 expression was reduced in the fibrotic group, while Gal-8 expression was increased in the ginger group and silymarin and ginger group. Tissue levels of nitric oxide (NO) and malondialdehyde (MDA) were markedly increased in the fibrotic group but decreased in the silymarin and ginger group. Additionally, tissue caspase-3 activity and antioxidant markers were decreased in the fibrotic group. However, these markers were increased in the silymarin and ginger group. Conclusions: Gal-8 is a diagnostic and/or prognostic glycoprotein for liver fibrosis. The combination of silymarin and ginger has protective liver action and reduces the severity and incidence of liver fibrosis.
Berberine treatment activated AMP-activated kinase signaling and reduced TGF-ß1 and Smad3 phosphorylation. Of note, the inhibitory effects of BBR on adipose tissue fibrosis were significantly blocked by AMPK inhibition with compound C, an AMPK inhibitor. Macrophage infiltration and polarization induced by HFD were also reversed after BBR administration. These findings suggest that BBR displays beneficial effects in the treatment of obesity, in part via improvement of adipose tissue fibrosis.