Effects of curcumin on lipid profile and lipid peroxidation status in experimental hepatic fibrosis

Guenzet, Akila; Rajakrishnan, V.; Viswanathan, P. N.; Rajashekaran, K.N; Menon, Venugopal P.

doi:10.1016/s1386-6346(98)00026-6

Cited by 39 publications

(18 citation statements)

References 19 publications

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“…The natural polyphenolic compound curcumin, known to be a strong antioxidant, occurs in the rhizomes of Curcuma longa Linnaeus (turmeric : Ammon & Walh 1991). It has been reported to have anti-in¯ammatory (Ammon & Walh 1991), anticarcinogenic (Rao et al 1995), liver-protective (Akila et al 1998;Chuang et al 2000;Park et al 2000a), antioxidant (Ruby et al 1995) and pulmonary-protective (Punithavathi et al 2000;Venkatesan 2000) eOE ects. It also inhibits the accumulation of collagen in the tail tendons and skin of diabetic rats (Sajithlal et al 1998).…”

Section: Introductionmentioning

confidence: 99%

“…We previously demonstrated that curcumin reduces the serum levels of alanine transaminase and aspartate transaminase, and reduces hydroxyproline and lipid peroxide contents in cases of liver injury induced by carbon tetrachloride (Park et al 2000a). Some other studies have also demonstrated that turmeric and}or curcumin inhibits liver injury (Kiso et al 1983;Donatus et al 1990;Akila et al 1998). However, direct evidence to support its eOE ect on HSCs during liver injury in-vitro or in-vivo is not yet available.…”

Section: Introductionmentioning

confidence: 99%

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Curcumin inhibits collagen synthesis and hepatic stellate cell activation in-vivo and in-vitro

Kang

Nan

Park

et al. 2002

Journal of Pharmacy and Pharmacology

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We previously demonstrated that curcumin, a well-known antioxidant, inhibits collagen deposition in carbon tetrachloride-induced liver injury in rats. The major effector cells responsibleforcollagensynthesis in the liver are activated hepatic stellate cells. In this study,we investigated the inhibitory effects of curcumin on the collagen synthesis and activation of rat hepatic stellate cells in-vitro, and on hepatic stellate cell activation in-vivo. The effects of curcumin on the production of collagen and smooth muscle alpha-actin proteins and of alpha1(I) collagen mRNA were studied in-vivo and in-vitro. The effect of curcumin on DNA synthesis was also determined in-vitro. In-vivo, treatment with curcumin reduced collagen deposition and smooth muscle alpha-actin-positive areas and lowered mRNA levels of type I collagen in the liver. In-vitro, curcumin at a concentration of 5 microg mL(-1) reduced DNA synthesis, and downregulated smooth muscle alpha-actin and type I collagen expression, and alpha1(I) collagen mRNA expression. We concluded that curcumin inhibits collagen synthesis and hepatic stellate cell activation in-vivo and in-vitro, and thus may prove a valuable anti-fibrogenic agent.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Curcumin inhibits collagen synthesis and hepatic stellate cell activation in-vivo and in-vitro

Kang

Nan

Park

et al. 2002

Journal of Pharmacy and Pharmacology

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“…In inflammatory conditions, the cytoplasmic membrane sustains the main damage; leakage of cytoplasmic contents causes a relatively greater increase in plasma ALT than AST. In infiltrative disorders, in which there is damage to both mitochondrial and cytoplasmic membranes, there is a proportionally greater increase in AST activity than ALT [24,25]. The AST/ALT ratio is used for differential diagnostic liver disease, while ratio <1 indicate mild liver damage, ratio>1 are associated with severe, after chronic liver disease.…”

Section: Discussionmentioning

confidence: 99%

Study on Blood Biochemical Diagnostic Indices for Hepatic Function Biomarkers in Endemic Skeletal Fluorosis

Shashi

Bhardwaj

2011

Biol Trace Elem Res

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The aim of the study was to determine the relationship of fluoride in drinking water to liver function in individuals living in normal and seven endemic fluorosis areas of Punjab, India. The concentration of fluoride in drinking water of different areas varied from 5.9 to 24.5 mg/L. Study group consisted of 705 patients in the age group between 20 and 60 years (mean age of 39.35±11.27) affected with osteodental fluorosis were compared with 300 age- and sex-matched controls (with mean age of 35.28±8.25 years). Biochemical data was analyzed by one-way analysis of variance (ANOVA) with post hoc Tukey-Kramer and Bonferroni multiple comparison tests. The relationship between hepatic enzymes was calculated by Pearson's correlation and linear regression. The results revealed significantly (P<0.001) higher concentration of serum fluoride in patients when compared to control. The mean activities of cyclic adenosine monophosphate (AMP), alkaline phosphatase (ALKP), acid phosphatase (ACP), aspartate aminotransaminase (AST), and alanine aminotransaminase (ALT) were significantly (P<0.05-0.001) elevated in patients from all fluoride areas. ANOVA with post hoc Turkey-Kramer and Bonferroni multiple comparison test demonstrated a significant (P<0.0001) variance in the activities of cAMP, ALKP, ACP, AST, and ALT in fluorotic patients, with elevation in water fluoride levels. Maximum elevation of 196.14% (ACP), 99.31% (cyclic adenosine monophosphate; cAMP), 72.08% (ALT), 60.14% (AST), and least 21.35% (ALKP) was recorded in patients exposed to 24.5 mg/L fluoride in drinking water. There was positive correlation between water fluoride, serum fluoride and AST (r=0.77, 0.91), ALT (r=0.82, 0.90), ALKP (r=0.88, 0.97), and ACP (r=0.74, 0.85). Pearson's correlation demonstrated highly significant (P<0.05) positive relationship between water fluoride and cAMP (regression equation: Y=0.9807×+22:081, =0.84; r=0.92, P<0.05). The increased levels of transaminases in fluorotic patients suggest alteration in liver functions. The level of alkaline and acid phosphatase was increased during fluoride intoxication which is also an early marker of hepatic cell damage because of its specificity and catalytic activity. The elevated levels of enzymes are reflective of bone disorders, which are characterized by increased osteoblastic activity. There levels increased several times if cellular damage occurs in the liver. The results suggest that fluoride exposure intensifies the activities of hepatic function enzymes in osteofluorosis.

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“…Data found in table (8) observed that a significant decrease (P<0.05) in SOD enzyme activity in the liver tissue of catfishes treated with concentration 5% and 10% pendimethaline for 7 and 21 days when compared with the control Under the stressful conditions, the catfish become hyperactive and thus require large amounts of oxygen to achieve the requirements of energy also, secrete large amounts of mucous to coat their body especially on the gills to gain relief from the irritating effects of toxicants ( As fish are in direct contact with the environment, only a thin epithelial membrane separates the blood of the fish from water (HlaveandBulkey, 1980). As a matter of fact, blood is a pathophysiological reflector of the body because it is highly susceptible to internal and external environmental fluctuations.…”

Section: Antioxidant and Oxidative Stress In Liver Tissue:-mentioning

confidence: 99%

Physiological and Oxidative Stress Biomarkers in the Freshwater Catfish(clarias Gariepinus) Exposed to Pendimethalin-Based Herbicide and Recovery With Edta.

Zaahkook¹,

El-Rasheid²,

Ghanem³

et al. 2016

IJAR

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Effects of curcumin on lipid profile and lipid peroxidation status in experimental hepatic fibrosis

Cited by 39 publications

References 19 publications

Curcumin inhibits collagen synthesis and hepatic stellate cell activation in-vivo and in-vitro

Curcumin inhibits collagen synthesis and hepatic stellate cell activation in-vivo and in-vitro

Study on Blood Biochemical Diagnostic Indices for Hepatic Function Biomarkers in Endemic Skeletal Fluorosis

Physiological and Oxidative Stress Biomarkers in the Freshwater Catfish(clarias Gariepinus) Exposed to Pendimethalin-Based Herbicide and Recovery With Edta.

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