Hepatic need liver transplantation (Bataller and Brenner, 2005).

fibrosis is a scarring mechanism related to prominent deposition of
extracellular matrix in the liver. Without efficient treatment at
early stage, reversible liver fibrosis becomes irreversible cirrhosis leads
to liver failure, portal hypertension and often need liver
transplantation (Bataller and Brenner, 2005). These progressive
scarring insults
in liver
cause cirrhosis, which is the foremost health burden leading
death worldwide
(Ismail and Pinzani,
present, no known therapeutic approach offered, except
removal of the fibrogenic stimuli, to heal this potentially overwhelming
in vivo and clinical studies have established that the liver fibrosis and cirrhosis are reversible to heal, but still inadequate known treatment (Klein et
al., 2006; Popov and Schuppan, 2009; Fink et al., 2011). This liver fibrosis is usually caused due to diverse
chronic insults including, chemicals, pesticides, parasitic infections,
viral hepatitis B and C, autoimmune hepatitis, and accumulation of toxic metals.
to the worldwide occurrence of these insults, liver fibrosis is widespread
and is related
linked morbidity and mortality (Sebastiani et al., 2014). Chronic
liver injury normally causes progressive liver fibrosis distinguished
by alterations
of both quality and quantity of hepatic extracellular matrix proteins
including collagen, which occurs in most types of end stage liver diseases (Al-Attar and Al-Rethea, 2017).  Furthermore, this chronic liver injury
is triggered by ROS and results from an unsuitable balance between the
production and clearance of ROS and leads to aberrant tissue damage in
(Ganesan et al., 2017).

Thioacetamide (TAA) is an
organosulphur chemical extensively used as a fungicide, as well as in various
industries including medicine and textile dye (Al-Attar and Al-Rethea, 2017). Presently, it is accounted as a carcinogen (Dweep
et al., 2017). It is metabolized in vivo
to free radical derivatives (TAA sulfoxide and TAA-S-S-dioxide) leads to lipid
peroxidation eventually culminates in centrilobular damage and liver injury (Bashandy
et al., 2017). Earlier studies have also been demonstrated that the exposure to
TAA caused liver injury, fibrosis, steatosis,
and cirrhosis in experimental animals (Lee et al., 2017; Matsuda et al., 2017;
Hussein et al., 2017; Kaur et al., 2017). Hence, TAA is recognized as a model
of liver fibrosis in rats.

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Currently, the treatment
of hepatic
disorders, including liver fibrosis and cirrhosis are inadequate; in
medicine, no effective therapy has been
preventing the development of hepatic diseases yet. Though recently developed drugs
have been used to heal liver diseases, often these drugs have numerous
side effects. It is, thus, urgently
required for alternative remedy or drugs for the treatment
of chronic
liver disorders to replace present drugs of uncertain
safety and effectiveness (Feng et al., 2017; Olugbami et
al., 2017). For this intention, herbal constituents and dietary
supplements are promising therapy as alternative medicines for the
treatment of chronic liver diseases and related metabolic derailments (Gupta
al., 2016; Naji et al., 2017; Rehman et al., 2017).

Justicia tranquebariensis L. (Family: Acanthaceae) is a common
shrub widely distributed in various regions of India, Malaysia, and Sri Lanka. The
fresh leaves are coolant and aperient, generally used in jaundice, liver
diseases, and smallpox (Nadkarni, 1976). Bruised leaves are applied to contusions,
diaphoretic, diuretic, and rheumatism and antidote for snake bite (Asolkar et
al., 2000; Sekhar et al., 2011). The leaf juices are used as an expectorant in cold,
cough, nasal disorders and the paste of the leaves is
applied externally to treat skin diseases, swelling and pain (Yoganarasimhan,
2000; Poongodi et al., 2011). The
root paste is also used to treat for a toothache (Sandhya et al., 2006). Phytochemical studies of J.tranquebariensis revealed the leaves
contain adequate quantities of phytosterols, flavonoids, glycosides,
triterpenoids, alkaloids, saponins, and
tannins (Akilandeswari et al., 2001a; Begum et al., 2008b). Aerial parts
of the plant
contain lignans including aryl
tetralin, ?-cubebin, lariciresinol,
isolariciresinol, lyoniresinol and medioresinol (Raju and Pillai, 1989). In
addition, the alcoholic extract of the plant yielded brassicasterol,
Campesterol, 7, 22–ergostadienol,
stigmasterol, sitosterol, spinasterol,
28-isofucosterol and ?-sitosterol-3-O-glucoside (Nadkarni, 1976). Further,
the plant has various pharmacological potentials including free radical
scavenging (Balamurugan et al., 2008), antimicrobial (Elayaraja et al., 2008;
Begum et al., 2008a), antipyretic (Begum et al., 2009), antihepatotoxicity (Sankaranaryanan,
1988; Begum et al., 2011), and anti-inflammatory activities (Akilandeswari et
al., 2001b). Based on the literature, no information was available on the hepatoprotective
and antioxidant effect of the J.tranquebariensis
leaf extract on liver fibrosis.
Hence the aim of the present study was to examine the hepatoprotective effect
J. tranquebariesis
on TAA-induced oxidative
stress and hepatic fibrosis in rats


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