STUDIES ON THE HEPATOPROTECTIVE EFFECT OF STOLEPHORUS COMMERSONNII FISH EXTRACT AND FLAVONOID RUTIN IN RATS
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Date
2023-03
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SRI VENKATESWARA VETERINARY UNIVERSITY TIRUPATI - 517 502. (A.P.) INDIA
Abstract
Liver plays a major role in the metabolism, detoxification and excretion of
xenobiotics. As a consequence, hepatocytes are exposed to high concentrations of these
toxic substances, which can lead hepatoxicity, liver dysfunction, and even total organ
failure. The main pathological pathway involved in majority of the liver disorders is
oxidative stress and its associated lipid peroxidation. Inspite of tremendous
advancements in modern medicine, natural antioxidants and hepatoprotective agents are
widely considered to be superior over conventional drugs due to the adverse effects
associated with the latter.
Experimentally, carbon tetrachloride (CCl4) is commonly used to induce
oxidative stress related liver injury in animals. Hepatotoxicity induced by CCl4 involves
the formation of trichlormethyl free radical (CCl3•) by cytochrome P-450 enzyme
system, that is further transformed to highly reactive trichloromethylperoxy radical
(CCl3OO•) in the presence of oxygen. This highly reactive radical then initiates a chain
reaction of lipid peroxidation by attacking polyunsaturated fatty acids, disrupts calcium
homeostasis and eventually kills cells. Stolephorus commersonnii is a marine water fish
enriched with high amounts of essential amino acids (lysine, isoleucine, threonine, and
serine), omega-3 polyunsaturated fatty acids (EPA, DHA), and minerals (iron, copper,
zinc, sodium, and potassium). It has been proven to possess several health benefits due
to its high nutritional and therapeutic significance. Rutin is a flavonol glycoside that is
widely distributed in nature in various vegetables and fruits such as the passion flower,
buckwheat, green asparagus, apple, oranges, onions and tea. It is known for its
antioxidant and inhibitory effects on generation of reactive oxygen species and
membrane lipid peroxidation. The current work was planned to study the
hepatoprotective effect of chloroform: methanolic extract of Stolephorus commersonnii
fish, flavonoid rutin, and their co-administration against CCl4-induced toxicity in adult
male Wistar albino rats.
The animals were randomly assigned to five equal groups, with six animals in
each. Group I (control) animals were treated with 1% DMSO (vehicle) orally for 3
weeks and olive oil @ 1ml/Kg b.wt. IP twice a week in 2
nd and 3rd week. Animals in
Group II which served as toxic model received CCl4 @ 1ml/Kg b.wt in olive oil (1:1) IP
twice a week in 2
nd and 3rd week. Group III animals were administered with Stolephorus
commersonnii fish extract (SCFE) orally @ 300 mg/Kg b.wt. in 1% DMSO for three
weeks, along with CCl4 as in Group II. Group IV animals were treated with rutin @
20mg/Kg b.wt. in 1% DMSO orally for 3 weeks along with CCl4 as in Group II.
Animals in Group V received CCl4 as in Group II, fish extract as in Group III, and rutin
as in Group IV.
Twenty-four hours post last treatment, all the animals were sacrificed by cervical
dislocation after retro-orbital blood collection. CCl4-induced hepatotoxicity toxicity in
toxic group rats was manifested as a decrease in body weight gain, an increase in ALT,
AST, ALP, total and direct bilirubin, BUN, and creatinine in serum, a decrease in
plasma total protein and albumin, decrease in antioxidant markers viz., SOD, CAT,
GPx, and GSH and increase in lipid peroxidation marker, TBARS. Alterations in gross
and histological architecture like fat deposition over liver surface, necrotic hepatocytes,
cloudy swelling, fatty changes and hydropic degeneration were evidenced.
Treatment with S. commersonnii fish extract and rutin either singly or in their
combination, significantly improved the body weight gain and reverted the biochemical
and histopathological alterations induced by CCl4. Though both fish extract and rutin
individually exhibited significant hepatoprotective effect, it appeared that their co-administration produced better protective effect.