Curcumin principal cytokine that cause tubulointerstitial fibrosis ( Wada

is a isolated polyphenol that from a long plant crcuma is commonly known as
turmeric ( kossler, etal.2012 ). Turmeric reported to have effective application in
various kinds of diseases such as asthma,fibrosis ( Zhang D , etal.2013 )
Curcmin is one of the active ingredient in turmeric that reduce  the expression of apaptotic and chemokines
genes in a model of  uretral obstruction ( Jones ,etal.2000) After 
performing various experiments study shows the effects and mechanism of
curcumin because curcumin has a potential source in the prevention and treatment
of renal fibrosis. Recent studies  also
shows that there is no toxicity 0f curcumin rising when it is taken at the
recomended dose which increased the potential of therapeutic agent. Currently
there are no effective drugs that helps in the prevention of end stage renal
disease .Curcumin dose reduce the parameters of fibrosis and associated with a
reduction in inflamatory mediators. Renal fibrosis consist of four phases in
the first stage of renal fibrosis inflammatory stimulation active the renal
tubualr epithelial cells and the infiltration of inflammatory cells including
lymphocytes, monocytes and mast cell (
Meng XM, etal.2014 ). Curcumin
control the multiple proinflammatory molecules and reduce the activation of
inflammatory macrophages ( kuvabaraa N, etal.2006 ) in various renal
fibrosis models.

Monocyte chemotactic protein is an important medium for the momocyte
infiltration and a principal cytokine that cause tubulointerstitial fibrosis ( Wada T, etal.2004 ). T macrophages attached to the site of injury by
MCP-1 and its receptor CCR2. Blockage of 
MCP-1 pathway  prevent the kidney
fibrosis and reduce the formation of M1 inflammatory macrophages ( Kitagawa K, etal.2000 ). Proinflammatory cytokines incudes TNF-a and IL-1B
these are the factors that are involved in the development of chronic kidney
disorders ( Kayama F, etal.1997 ). High levels of these
factors contribute to inflammation and curcumin reduced the levels of these
factors. Curcumin and its analogs have the strong ability of anti-inflammation.
Curcumin is a component of turmeric that is non toxic and have a antioxidant activity.
Heme oxygenase-1 is the activated form of the rate limiting enzyme that is
involved in the degradation of heme.  It
is responsible for converting heme to carbon monoxide and free iron( Agarwal A, etal.2002). Heme oxygenase-1 is strongly activated by
oxidative stress and shows cytoprotective effects by the anti-inflammatory,
anti-apoptotic, and anti-proliferative actions ( Adin.CA, etal.2006).
The cytoprotective role of  Heme
oxygenase-1 linked to a modulation of the inflammatory process present in

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  It has been
proposed that blockage of the renin-angiotensin-aldosterone system (RAS) is the
most effective way to reduce fibrosis (Cassis
P,etal.2003). It is a
cytoprotective molecule that restore the renal functions via resolving fibrosis
factors ( X.Chen, etal.2016).
Curcumin treatment  also increased the
expression of  heme oxygenase-1 and the
results shows that hem oxygenase-1 may offer the new opportunities for the
renal disease treatments.Curcumin also exhibit anti- inflamation  properties in different kidney disease models
by decreasing  inflammatory molecules.

fibrosis is a common feature that  cause
the  kidney disease.Development of renal
fibrosis lead to the loss of renal function(
Eddy AA,etal.2005).Tubulointerstitial
 fibrosis is the pathway of renal
fibrosis. Tubulointerstitial fibrosis is epithelial mesenchymal transition (
EMT)  ( Zeisberg, etal.2004)  Epithelial to mesenchymal change  involving injured epithelial cells plays an important
role in the development of  fibrosis in
the kidney. Tubular epithelial cells can develop a mesenchymal phenotype that
increased  migratory capacity and  enables them to move from the renal tubular
microenvironment into the interstitial space and clear the potential apoptotic
cell death. Epithelial mesenchymal change  is a major contributor to the pathogenesis of
renal fibrosis as it leads to a considerable  increase in the number of myofibroblasts.
However  recent findings suggest that
epithelial mesenchymal change  involving
tubular epithelial cell that is a reversible process and potentially determined
by the surviving cells to facilitate the repopulation of injured tubules with
new functional epithelia. TGF-?1 is a well-established  activator of  epithelial mesenchymal change that  involving renal tubular epithelial cells.
Experiments indicate that curcumin prevented epithelial mesenchymal change
through increasing the expression of 
epithelial cadherin and reducing the expression of  mesenchymal smooth  muscle (
X.C.Liu, etal.2014) .Curcumin  also inhibit 
the occurence of epithelial mesenchymal change  in renal tubular epithelial cells .Curcumin
treatment increased the antioxidant profiles and decreased the oxidant  profile in the kineys and curcumin may also
show  the 
renoprotective  effect through  Nrf2. Nrf2 
also show  cytoprotective effect
through binding to the  antioxidant  response 
elements. Renal injury get better through the  curcumin treatment  by decreasing 
glutathione S-transferase immunoreactivity  which 
indicate that exogenous 
antioxidant curcumin compensate the need of renal cells to the
endogenous glutathione antioxidant (
W.Wang etal.2015 ).

growth factor-? (TGF-?) proteins regulate the cell function . The intracellular
effectors of  Transforminf growth factor-?
signalling the Smad proteinsthat  are
activated by receptors and translocate into the nucleus  where they control the transcription.  Signalling pathways further  control Smad activation and function..  Transforming growth factor  is the major activator of  epithelial mesenchymal change and it is
activated through smad dependent and smad independent pathways ( Zhang,etal.2003
).Transforming growth factor  and
smads signals is the most important pathway in the development of renal
fibriosis.Curcumin treatment  inhibit the
transforming growth factor  expression
and this inhibitory effect reduce the phosphorylation of  smad.Curcumin treatment decreased the
expression of collagen ( X.Y.Fu,etal.2015).

       The MAPK is a
signalling pathway that is involved in the development of renal  fibrosis. Pretreatment with curcumin blocked
the angiotensin II  that is the activator
of profibrotic responses in renal tubular epithelial cells .At the activation stage of renal fibrosis curcumin treatment
inhibit the epithelial mesenchymal change and rebuilds the antioxidant
balance.Curcumin also shows the antifibrtogenic properties by blocking the MAPK
.Curcumin is beneficially involved in the treatment of renal fibrosis at the primary
activation stage through preventing the inflammation, rebuild the redox balance
and inhibit the epithelial mesenchymal change. These are the actions that
reduce inflammation factors and activate the expression of anti-inflammation
factors that targets the TGF-b, MAPK pathways.

play a protective role in th


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