Looking at another herbal therapy, Anping Chen and colleagues presented 3 laboratory studies assessing at the effect of curcumin on hepatic stellate cells.
Curcumin is the main component of the curry spice turmeric, derived from the Curcuma longa plant. Prior research indicates that it has antioxidant, anti-inflammatory, and anti-tumor properties. Hepatic stellate cells produce extracellular matrix proteins such as collagen that are responsible for liver fibrosis.
In the first study, the investigators found that curcumin promotes peroxisome proliferator-activated receptor-gamma (PPAR-gamma) gene expression and suppresses expression of the low-density lipoprotein (LDL) cholesterol receptor gene, which in turn lowers the level of intracellular cholesterol and thereby reduces the stimulatory effect of LDL on hepatic stellate cell activation.
In the second study, the researchers demonstrated that curcumin diminished the activating effect of oxidized LDL on stellate cells by suppressing LOX-1 gene expression, again via PPAR-gamma activation. Conversely, pre-treating the cells with a PPAR-gamma antagonist (PD68235) eliminated the inhibitory effect of curcumin.
Finally, the investigators showed that by increasing oxidative stress, insulin stimulates hepatic stellate cell proliferation and collagen production. But curcumin suppressed insulin-induced stellate cell activation by interrupting the insulin signaling pathway and reducing oxidative stress, via the same PPAR-gamma mechanism.
Hyperlipidemia (elevated blood lipid levels), obesity, and insulin resistance are features of the metabolic syndrome, which is associated with liver steatosis (accumulation of fat in hepatocytes). Steatosis is linked to fibrosis in individuals with non-alcoholic fatty liver disease, as well as those with chronic hepatitis C. Further, steatosis and insulin resistance are factors associated with poor response to interferon-based anti-HCV therapy.
The results of these laboratory studies suggest that curcumin or related agents that work by a similar mechanism might reduce fibrosis associated with hyperlipidemia or insulin resistance in individuals with or without hepatitis C. "
Stopped taking Curcumin prior to tox as it is an antiinflammatory. Now that I have become insulin resistant, would curcumin now be a benefit as an additive to my regimen?
i've heard some good things about curcumin/ tumeric. i think mainly used spice among the Indian populations originated in India and studies have shown that elderly people who used this spice significantly within their life time had reduced troubles with cancer. some sources have also suggested that it may prevent cancer as well.
i'm currently txing and don't know much about drug interaction so i'm not going to risk taking it as of now. but, some of my family members have already tried some.
possibly consider taking it when you are not on tx.
of topic got to ask you this you the only one that says tox instead of tx, tox make me think of toxin maybe you the one how have the most accurate formulation.
Anyway just curious.
You have commed far and you have responded I´m not sure about this but the studies I`ve read about giving metformin to HCV, IR patients is to make them respond faster to meds and by doing so increase the SVR rate.
In other words I´m not sure IR are such a big issue once you have got to UND but that could be a question that maybe CS or CO can answer.
I also was taking it before I started TX. I stopped all sups until after I'm done TX and will go back on Curcumin, revesterol, and a few others. That is great that it helps with Insulin Resist but what concerns me is if it lowers LDL. There was some studies awhile back that a higher LDL actually helps with TX and SVR.
I was using curcumin spice on everything before starting tx. I'd sprinkle it on my sandwiches, in my tea etc. In Indonesia, where I lived for 20 years, it is common knowledge to use it when people have anything with the liver. They've done that for centuries. I am not taking it like that anymore, since starting tx.
Among its many effects, curcumin has a blocking effect on activation of NFKappaB, the universal cellular stress sensor that indirectly activates numerous pro inflammatory genes, in particular Tumor necrosis Factor alpha, TNFalpha. Therefore, as discussed earlier, since the proinflammatory effects might be helpful in suppressing viral replication it might not be a good idea during tx, regardless of its antifibrotic effects and other positive effects like counteracting IR. Wait until all treatment has stopped, posssibly until SVR is confirmed.
I stopped taking it after more reading, what HR said.....and plus....you gotta be mexican to not feel the burn on this stuff : )))))))))))))))))))). It might work wonders in some areas but in burns like hellfire in others...if you catch my drift.
Outside of tx however Curcumin is likely one of the very top antifibrotic agents. Numerous in vitro studies with activated stellate cells ( that produce fibers in their state of "Myofibroblasts") habe shown an inhibitory effect of Curcumin on this process of stellate cell activation and transdifferentiation. Unfortunately we do not have in vivo human studies to confirm this effect, there is no commercial interest to fund such studies.
Here is yet another recent study to show the effectiveness of curcumin in reversing hepatic stellate cell activation:
Indian J Biochem Biophys. 2008 Oct;45(5):317-25.
Curcumin-induced recovery from hepatic injury involves induction of apoptosis of activated hepatic stellate cells.Priya S, Sudhakaran PR.
Department of Biochemistry, University of Kerala, Kariavattom, Thiruvananthapuram, India. ***@****
Hepatic stellate cells (HSCs) undergo activation and transdifferentiation to myofibroblast like cells in liver injury, leading to liver fibrosis.
During recovery from injury, activated HSCs may either revert back to quiescent state or undergo apoptosis or both. In the present study, we have examined whether recovery from hepatic injury involves apoptosis of activated HSCs and tested whether curcumin (the yellow pigment from Curcuma longa Linn.) promotes recovery from hepatic injury by inducing apoptosis of these cells.
Hepatic injury was induced by CCl4 and apoptosis was studied in HSCs isolated from liver by MTT assay, DNA fragmentation, and DAPI and annexin staining. Hepatic recovery was assessed by measuring hepatic marker activities, such as serum GOT, GPT and protein.
Hepatic recovery occurred within 4 weeks after inducing injury in untreated control, whereas curcumin treatment caused hepatic recovery within 2 weeks, as evidenced by the reduction of hepatic marker activities to near normal levels.
HSCs isolated from liver of animals treated with curcumin showed maximum apoptotic marker activities in 2nd week, whereas in HSCs from untreated control recovering from injury, maximum apoptosis was observed in 4th week. Induction of apoptosis in vivo during hepatic recovery was also suggested by increase in caspase-3 activity. Treatment of isolated HSCs in culture with curcumin caused apoptosis during later stages confirming that curcumin induced apoptosis of activated HSCs and not in unactivated quiescent HSCs.
These results suggested that hepatoprotective effect of curcumin causing recovery from injury involved apoptosis of activated HSCs.
I am so grateful for every tid bit you throw our way. After 24 weeks of pegasys, 1400 riba, and alinia, Joe was still detectible with a viral load of 250. We will continue on meds until the end of feb. and hope for a miracle, but we know what to do if it doesn't happen...we will run back to your supplement list. This was Joe's 3rd try and he has cirrhosis. Your supplement list was the only thing that got him well enough to be considered for another tx attempt.
With a thankful heart,
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