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Cirrhosis – dissolve the scar tissue with enzymes


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#1 Fred C. Dobbs

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Posted 17 August 2015 - 07:22 AM

Cirrhosis is the replacement of normal liver tissue by scar tissue (fibrosis), made up of fibrous connective tissue such as the protein collagen.


Nattokinase and Serrapeptase are proteolytic (protein-digesting) and fibrolytic (fibrin-digesting) enzymes.


  1. Would these enzymes (or bromelain) be effective at dissolving Cirrhosis scarring?
  2. Which do you think is best?
  3. What do you think is a good dosage?
  4. Is there any significant difference between these enzymes?
  5. Bonus question: Will these enzymes dissolve gallstones?

Serrapeptase is the silkworm enzyme.  It is a kinase, which is a type of enzyme that catalyzes the transfer of phosphate groups from high-energy, phosphate-donating molecules to specific substrates.  Protein kinases act on proteins, phosphorylating them on their serine, threonine, tyrosine, or histidine residues.


Nattokinase is the fermented soybean enzyme, produced using the bacterium Bacillus Subtilis natto. It is not a kinase enzyme. It is a serine protease, which is a type of enzyme that cleaves peptide bonds in proteins, in which serine serves as the nucleophilic amino acid at the (enzyme's) active site. Nattokinase indirectly increases urokinase and plasmin.



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#2 Matman32

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Posted 17 August 2015 - 10:41 AM

I'm wondering the same thing about gut scar as I have some stricturing due to Crohn's disease! I've started eating natto each morning since I came back from a Japan trip, it grows on you hehe. 

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#3 Dolph

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Posted 17 August 2015 - 11:13 AM

Cirrhosis is already associated with coagulopathy. Taking something like nattokinase would be a good way to shorten your life and bleed to death, especially if esophageal varices have already developed!

There is no way to "dissolve" scar tissue and even if that worked it wouldn't be a solution. The problem is the lack of healthy liver tissue.

Edited by Dolph, 17 August 2015 - 11:14 AM.

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#4 ceridwen

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Posted 17 August 2015 - 12:25 PM

The liver regenerates itself if a healthy diet can be followed and that's not the only thing. That following a healthy diet though can be really difficult
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#5 Fred C. Dobbs

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Posted 18 August 2015 - 03:36 AM

"There is no way to "dissolve" scar tissue..."


In the product reviews for Serrapeptase on Amazon.com, there are a lot of reviews that report success with dissolving scars.

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#6 Fred C. Dobbs

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Posted 18 August 2015 - 03:21 PM

Thanks for the info on coagulopathy in cirrhosis patients.


How acute is the coagulopathy? If it is  already very severe, the serrapeptase might not make much difference.


There is risk taking serrapeptase, but there is also risk with getting a liver transplant or with doing nothing or with waiting for a transplant that never happens.


What is a remedy for coagulopathy for someone with cirrhosis taking serrapeptase? Take K2? Increase platelet count?


Compared to Nattokinase, Serrapeptase has far more reviews (a huge number) reporting that it dissolved internal and external scars, so I am focusing on that enzyme for now.




#7 zorba990

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Posted 18 August 2015 - 11:02 PM

From recent research for someone, I would look at (in addition to addressing the primary cause , e.g. hepatitis, alcoholism or binge drinking, other inflammatory issues):

European Milk Thistle





C60 may be of help but studies are still limited...

#8 niner

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Posted 19 August 2015 - 01:02 AM

there are a lot of reviews that report success with dissolving scars.


Are these some kind of special "scar" that isn't really a scar?  Honest-to-God scar tissue is pretty intractable stuff.  I don't think even SENS has an answer for scar tissue, other than 'live long enough for science to figure out how to grow new body parts'.  There are a lot of claims that you can "dissolve" uterine fibroids with enzymes, but they are not the same thing as scar tissue.  They are known to shrink when estrogen levels drop.  I wish I could dissolve scar tissue, because it's at the root of my tendinopathy, among other things.  Along with dissolving it, you would need to replace it with properly ordered tissue.  It's a tall order.

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#9 Fred C. Dobbs

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Posted 19 August 2015 - 04:40 AM



Are these some kind of special "scar" that isn't really a scar?

In most cases, yes.


I analyzed Amazon.com reviews for the top 18 single-ingredient Serrapeptase products.


Out of 1221 reviews, 87 used the word "scar" or "scars."


Many of these reviews stated that the writer intended to use the product for a scar, or they described that the product is generally intended for scars. These reviews did not describe success with treating scars, or they were vague.


I counted 25 reviews that described success by the reviewer with scars.

  • Seven specified surgery scars (mastectomy, hysterectomy, facelift, 2 for heart surgery, 2 without details).
  • Four specified keloids.
  • Others mentioned burns, internal scars (e.g., around the tendon), hidradenitis suppurativa, injuries, Peyronie, old scars

In addition to those 25  "real scars," there were 3 more that claimed the Serrapeptase removed scar tissue and thereby unblocked Fallopian tubes. By the description, it sounds like it may have been something other than true scar tissue blocking the tubes.

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#10 Fred C. Dobbs

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Posted 23 August 2015 - 08:53 AM

Most coagulation factors are produced by the liver, and thus, coagulopathy correlates with worsening liver disease.


Even so, anti-coagulants like Heparin are sometimes used safely in cirrhosis patients to avoid thrombosis.


In contrast to anti-coagulants, Serrapeptase lyses pre-existing thrombus -- possibly without significantly inhibiting clotting factors, which would make it a safer alternative to anti-coagulants.





A limited number of nonrandomized  studies  have evaluated the risks and benefits of anticoagulation therapy in cirrhotic patients with portal venous thrombosis. In one series, treatment with anticoagulation therapy resulted in an overall response rate of 60%[226]. Another study found that 75% of the patients treated with low molecular weight heparin (LMWH) for a median time of 11 mo achieved complete recanalization[227]. Preliminary results from a prospective randomized trial suggest that daily low dose LMWH can prevent PVT inpatients with cirrhosis without significant increase in risk of bleeding. In addition prophylactic use of LMWH decreased the incidence of  hepatic decompensation[228].


Vitamin K deficiency is commonly seen in cases of decompensated liver cirrhosis. Vitamin K 10 mg injections administered for three days are considered  adequate to correct the vitamin K deficiency and should be given to patients with decompensated liver cirrhosis[229]. In cases with acute bleeding, transfusion of platelets and fresh frozen plasma can be considered for patients with thrombocytopenia and coagulopathy[145].


Nattokinase does function as an anti-coagulant but still might be safer than alternatives like Heparin and is worthy of consideration.





45 subjects took 4000 fibrinolysis units of Nattokinase per day over 2  months. This results were as follows:

  • fibrinogen plasma levels decreased 7-10%
  • factor VII plasma levels decreased 7-14%
  • factor VIII plasma levels decreased 17-19%
  • blood lipids were unaffected








Edited by WmChurch, 23 August 2015 - 09:34 AM.

#11 IWS

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Posted 25 August 2015 - 08:39 AM

Hello WmChurch, Nattokinase is mainly used for arterial plaque and thrombus, most of research and testing made in Japan, Serrapeptase also used for the same plus the anti inflammatory properties, Dr. Hans Alfred Nieper did studies and experimentation with it, both lower blood pressure etc.


The 'scars' in liver cirrhosis you are referring to are not the same as the scars one is used to see, for example on the skin. You must think of them as an indelible sign of a degenerative process, not something you can remove, smooth or flat to restore liver funcionality. It's a whole condition which usually starts as an inflammatory process due to internal (steatosis) or external (hepatitis, alcohol, drugs, poisoning, contamination, etc.) factors, and which evolves into tissue degeneration and leads to the necrosis.


If you are able to remove the source of inflammation (viruses, alchol, etc.) you could be able to stop the degenerative process and recover/restore some of the liver funcionality. The main issue of the above process is that the stellate cells, usually used as storage (for fat soluble vitamins for example), stop storing and start over-producing collagen which leads to an abnormal liver density, source of the most of the cirrhosis complications as portal hipertension, splenomegaly, low platelet counts, esophageal varices, bleeding, etc.


IMO the pathway is 1) fight the inflammation, 2) lower blood pressure and promote blood circulation, micro-circulation, vasodilatation, NO as endogenous nitric oxide, etc., 3) induction of apoptosis of hepatic stellate cells. Not to mention that people with liver cirrhosis have a variety of conditions/deficiencies you should approach globally. Nattokinase and Serrapeptase could help in promoting overall blood circulation and plaque/thrombus removal but these are just a piece of the puzzle. There are supplements, herbs and stacks which can really help. For the above 1) you can look at Vitamin C, E, D, NAC, Curcuma, Boswellia, etc., for the 2) propranolol, nitroglicerin, nitrates, etc., for 3) nicotinamide etc. Just to mention something more the FZHYC is an herbal compound effective against fibrosis as well as many other products (as the mitoQ ability to reduce intrahepatic resistance as reported in another thread on this board).


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#12 alc

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Posted 25 August 2015 - 05:31 PM

@ WmChurch - for liver fibrosis you can look at:


1. FibroGen




2. Galectin Therapeutics




also Mesoblast are developing therapies for chronic inflammation:




in general there is a lot of work in regenerative medicine in these fields - look @ Alliance for Regenerative Medicine:






#13 Logic

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Posted 20 March 2016 - 01:12 PM

Nilotinib reduces muscle fibrosis in chronic muscle injury by promoting TNF-mediated apoptosis of fibro/adipogenic progenitors.
"...we show that in acutely damaged skeletal muscle, sequential interactions between multipotent mesenchymal progenitors and infiltrating inflammatory cells determine the outcome of the reparative process.
We found that infiltrating inflammatory macrophages, through their expression of tumor necrosis factor (TNF), directly induce apoptosis of fibro/adipogenic progenitors (FAPs). In states of chronic damage, however...macrophages express high levels of transforming growth factor β1 (TGF-β1), which prevents the apoptosis of FAPs and induces their differentiation into matrix-producing cells. Treatment with nilotinib, a kinase inhibitor with proposed anti-fibrotic activity, can block the effect of TGF-β1 and reduce muscle fibrosis....
Our findings reveal an unexpected anti-fibrotic role of TNF and suggest that disruption of the precisely timed progression from a TNF-rich to a TGF-β-rich environment favors fibrotic degeneration of the muscle during chronic injury."
There's a group buy on Nilotinib closing tonight:

#14 Heisok

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Posted 20 March 2016 - 07:59 PM

Does the liver have muscle cells?  Regardless of that would the process which they say effected muscles, translate to other tissue types?

#15 Heisok

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Posted 21 March 2016 - 12:44 AM

Found a study.


"Inhibition of PDGF, TGF-β, and Abl signaling and reduction of liver fibrosis by the small molecule Bcr-Abl tyrosine kinase antagonist Nilotinib"


"These studies uncover a novel role of Bcr-Abl activity in treatment of liver fibrosis through multiple mechanisms and indicate that Nilotinib represents a potentially effective antifibrotic agent."



#16 Logic

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Posted 21 March 2016 - 10:58 AM

Found a study.
"Inhibition of PDGF, TGF-β, and Abl signaling and reduction of liver fibrosis by the small molecule Bcr-Abl tyrosine kinase antagonist Nilotinib"
"These studies uncover a novel role of Bcr-Abl activity in treatment of liver fibrosis through multiple mechanisms and indicate that Nilotinib represents a potentially effective antifibrotic agent."

Good find heisokday.
Yes it seems that fibrosis in the liver, and generally, occurs because the  macrophages that should be killing off fibro/adipogenic progenitors (FAPs) by expressing TNF, also express too much TGF-β1 
which prevents the apoptosis of FAPs and induces their differentiation into matrix-producing cells.
It sees that Nilotinib blocks this excess TGF-β, bcl-2, DGF etc.

The question now is at what dosage does Nilotinib have this effect?
gives the full paper (any paper, but a 'spotty' server I think)
From the paper:

"The in vivo antifibrotic efficacy of Nilotinib was assessed in mice with liver fibrosis induced by Carbon Tetrachloride  and bile duct ligation" were dosed with:

50 mg/kg/day for 17 weeks.
HED (mg/kg) = Animal Dose (mg/kg) x [Animal Km / Human Km]
Human Km = 37
Mouse Km = 3
Rat Km = 6
50mg/kg x 3/37= 4.05mg/kg
So for a 70 kg Human Equivalent Dose is 284 mg/kg/day

That is within the dosages used in the Parkinson's study (150-300  mg/day) at which no side effects were noted?, but on the high side.

Also Nilotinib seems to be a liver protectant:
In conclusion, our data demonstrate that treatment with a tyrosine kinase inhibitor Nilotinib markedly attenuated development of liver fibrosis through multiple mechanisms bothin vitro and in vivo, including induction of HSC apoptosis, inhibition of PDGF, TGF-b, and multiple signal pathways, as well as suppression of neo-angiogenesis. In addition, a hepatoprotective activity of Nilotinib is apparent based on the reduction in transaminases and TBil, which offers an additional therapeutic advantage of Nilotinib, since it could both improve hepatocyte integrity while reducing stellate cell activation as two independent but complementary activities. Our study under-scores the rationale for the therapeutic trials of Nilotinib alone or in combination with other antifibrotic therapies for patients with liver fibrosis.

Note that the liver was challenged with highly toxic Carbon Tetrachloride in this study and a restorative effect, at lower doses, may be expected when NOT trying to poison the liver!?

#17 bossmanglb

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Posted 22 March 2016 - 05:15 AM

Are there any approaches relevant for treating fibrotic kidney tissues/scarring? 


#18 Logic

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Posted 23 March 2016 - 04:49 PM

Are there any approaches relevant for treating fibrotic kidney tissues/scarring?

Did you miss my above posts!?

#19 bossmanglb

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Posted 24 March 2016 - 10:14 PM

Sorry, but I didn't/dont' see the word kidney mentioned once   :unsure:

The posts seem to be about liver related fibrosis, no?

#20 Logic

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Posted 25 March 2016 - 08:24 AM

Sorry, but I didn't/dont' see the word kidney mentioned once   :unsure:

The posts seem to be about liver related fibrosis, no?


Oops!  My bad.   :)


Nilotinib Attenuates Renal Injury and Prolongs Survival in Chronic Kidney Disease



Fibrosis, Regeneration, and Aging: Playing Chess with Evolution





More general:

Present and Future in the Treatment of Diabetic Kidney Disease



Tyrosine kinase inhibitors for the treatment of fibrotic diseases such as systemic sclerosis: towards molecular targeted therapies


Edited by Logic, 25 March 2016 - 08:40 AM.

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#21 bossmanglb

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Posted 25 March 2016 - 04:00 PM

My profound thanks, Logic!!

#22 stefan_001

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Posted 25 March 2016 - 07:48 PM

This also seems interesting:

Researchers link absence of protein to liver tissue regeneration


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#23 Dorian Grey

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Posted 26 March 2016 - 05:11 AM

Halting production of additional fibrosis may be half the battle...  Stop laying down new fibrosis and allow the liver to begin healing itself.  




Effect of genistein and quercetin on proliferation, collagen synthesis, and type I procollagen mRNA levels of rat hepatic stellate cells.


"CONCLUSION: GE and QU inhibited hepatic stellate cell proliferation and collagen synthesis that might have a protective role against liver fibrosis"




Curcumin: potential for hepatic fibrosis therapy?

"The beneficial antioxidative, anti-inflammatory and antitumorigenic effects of curcumin have been well documented in relation to cancer and other chronic diseases. Recent evidence suggests that it may be of therapeutic interest in chronic liver disease. Hepatic fibrosis (scarring) occurs in advanced liver disease, where normal hepatic tissue is replaced with collagen-rich extracellular matrix and, if left untreated, results in cirrhosis. Curcumin inhibits liver cirrhosis in a rodent model and exerts multiple biological effects in hepatic stellate cells (HSCs), which play a central role in the pathogenesis of hepatic fibrosis. In response to liver injury, these cells proliferate producing pro-inflammatory mediators and extracellular matrix. Curcumin induces apoptosis and suppresses proliferation in HSCs. In addition, it inhibits extracellular matrix formation by enhancing HSC matrix metalloproteinase expression via PPARγ and suppressing connective tissue growth factor (CTGF) expression. In this issue, Chen and co-workers propose that curcumin suppresses CTGF expression in HSC by inhibiting ERK and NF-κB activation. These studies suggest that curcumin modulates several intracellular signalling pathways in HSC and may be of future interest in hepatic fibrosis therapy."


Coffee Anyone?  http://www.ncbi.nlm....pubmed/23808892


Caffeine attenuates liver fibrosis via defective adhesion of hepatic stellate cells in cirrhotic model

"Caffeine increased HSCs apoptosis and intracellular F-actin and cyclic adenosine monophosphate expression. Caffeine also inhibited procollagen type Ic and α-SMA expression in a dose- and time-dependent manner. In rat model, caffeine decreased periportal inflammation, levels of inflammatory cells (1.4 ± 0.52 vs 2.6 ± 0.46, P < 0.05), and fibrosis (2.1 ± 0.35 vs 2.9 ± 0.84, P < 0.05). Transforming growth factor-β and α-SMA expressions were also reduced by caffeine.


Caffeine attenuates the progression of liver fibrosis by inhibiting HSCs adhesion and activation."


And of course, keep iron low (through chelation or blood donation) to avoid progression of disease!  The liver is the primary storage site for excess iron, & iron is the flam in liver inflammation!  Give these titles a google for more on this.  


Iron-dependent activation of NF-kappaB in Kupffer cells: a priming mechanism for alcoholic liver disease


Iron Overload: An Important Co-Factor In The Development of Liver Disease in Alcoholics


Iron accumulation in alcoholic liver diseases


The Role of Iron in Alcoholic Liver Disease


Liver Iron is Predictive of Death in Alcoholic Cirrhosis


Serum ferritin concentration predicts mortality in patients awaiting liver transplantation




Iron chelators and iron toxicity


"Iron chelation may offer new approaches to the treatment and prevention of alcoholic liver disease. With chronic excess, either iron or alcohol alone may individually injure the liver and other organs. In combination, each exaggerates the adverse effects of the other. In alcoholic liver disease, both iron and alcohol contribute to the production of hepatic fibrosis through their effects on damaged hepatocytes, hepatic macrophages, hepatic stellate cells, and the extracellular matrix. The pivotal role of iron in these processes suggests that chelating iron may offer a new approach to arresting or ameliorating liver injury"


"These agents may provide new pharmacological means of averting or ameliorating liver damage in alcoholic liver disease by binding, inactivating, and eliminating the reactive forms of iron that contribute to oxidative injury of cellular components, are involved in signal transduction, or both."


Helpful Hints: Curcumin and Quercetin are both iron chelators.


Iron chelation in the biological activity of curcumin

"Consistent with the hypothesis that curcumin acts as an iron chelator, mice that were fed diets supplemented with curcumin exhibited a decline in levels of ferritin protein in the liver. These results suggest that iron chelation may be an additional mode of action of curcumin."


Role of Quercetin on iron homeostasis

"after longer oral treatment with quercetin, animals became iron deficient as both liver and spleen iron levels decreased significantly"

Edited by synesthesia, 26 March 2016 - 05:34 AM.

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#24 Mark4124

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Posted 19 July 2019 - 02:20 PM

I like the thought about dasatinib and nilotinib idea, but the concern I have is that these drugs are cardiotoxic and in some cases have even caused pulmonary hypertension, a very severe disease that generally leads to death. Thoughts on this concern? I am aware of curcumin and quercetin, but hadn't seen the combination with genistien before. Thanks for that, interesting.

#25 Puppalupacus

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Posted 19 July 2019 - 05:08 PM

Took Serrapeptase and Nattokinase for over a year consistently.  Did jack shite for scar tissue.

Edited by Puppalupacus, 19 July 2019 - 05:09 PM.

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#26 pamojja

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Posted 20 July 2019 - 11:36 AM

In my doctors report it read: "2 non-circulated nodules on the right edge of the liver (5 + 8mm)" found during sonography. Don't know if that already could have been scar tissue, it however dissolved after some years on my protocol without Serrapeptase and Nattokinase.

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