Potential preventive effect of carvacrol against diethylnitrosamine-induced hepatocellular carcinoma in rats

Jayakumar, Subramaniyan; Arumugam, Madan Kumar; Asokkumar, Selvamani; Raghunandhakumar, Subramanian; dhas, Krishnan Gokula; Kamaraj, Sattu; Divya, M.; Devaki, Thiruvengadam

doi:10.1007/s11010-011-1043-7

Cited by 176 publications

(154 citation statements)

References 40 publications

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“…In the respiratory system, CAR treatment decreases MDA and shows a significant protective role (Boskabady and Jalali 2013). CAR also prevents lipid peroxidation, cell damages, and protects the antioxidant system in diethylnitrosamine-induced liver cancer in male Wistar albino rats (Jayakumar et al 2012). It has also been reported that isoprenoids such as CAR, via posttranscriptional actions, suppress 3-hydroxy-3-methylglutaryl CoA (HMG-CoA) reductase activity in liver, the rate limiting enzyme for the synthesis of MDA (Akkol et al 2012).…”

Section: Discussionmentioning

confidence: 99%

The carvacrol ameliorates acute pancreatitis-induced liver injury via antioxidant response

et al. 2015

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Acute pancreatitis (AP) may cause significant persistent multi-organ dysfunction. Carvacrol (CAR) possesses a variety of biological and pharmacological properties. The aim of the present study was to analyze the hepatic protection of CAR on AP induced by cerulein and to explore the underlying mechanism using in vivo studies. The rats were randomized into groups to receive (1) no therapy; (2) 50 lg/kg cerulein at 1-h intervals by four intraperitoneal injection (i.p.); (3) 50, 100 and 200 mg/kg CAR by one i.p.; and (4) cerulein ? CAR after 2 h of cerulein injection. 12 h later, serum was provided to assess the blood AST, ALT and LDH values. Also, liver tissues were obtained for histological and biochemical measurements. Liver oxidative stress markers were evaluated by changes in the amount of lipid peroxides measured as MDA and changes in tissue antioxidant enzyme levels, SOD, CAT and GSHPx. Histopathological examination was performed using scoring systems. Oxidative damage to DNA was quantitated in studied tissues of experimental animals by measuring the increase in 8-hydroxydeoxyguanosine (8-OHdG) formations. We found that the increasing doses of CAR decreased pancreatitisinduced MDA and 8-OH-dG levels. Moreover, the liver SOD, CAT and GSH-Px activities in the AP ? CAR group were higher than that of the rats in the AP group. In the treatment groups, AST, ALT and LDH were reduced. Besides, necrosis, coagulation and inflammation in the liver were alleviated (p \ 0.05). We suggest that CAR could be a safe and potent new drug candidate for treating AP through its antioxidative mechanism of action for the treatment of a wide range of disorders related to hepatic dysfunction.

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Section: Discussionmentioning

confidence: 99%

The carvacrol ameliorates acute pancreatitis-induced liver injury via antioxidant response

et al. 2015

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“…Moreover, the resistance against hydrogen peroxide-induced DNA damage in hepatic and testicular tissues is higher in rats given CAR (Slamenova et al 2008). Besides, the potent free radical scavenger activity of CAR is demonstrated in hepatocellular carcinogenesis (Jayakumar et al 2011).…”

Section: Discussionmentioning

confidence: 99%

Carvacrol modulates oxidative stress and decreases cell injury in pancreas of rats with acute pancreatitis

et al. 2015

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Acute pancreatitis (AP) is considered as major problem around the world and the incidence of AP is increasing. Carvacrol (CAR), a monoterpenic phenol, has good antioxidant activity. This in vivo study was designed to evaluate whether CAR provide protection against AP that developed by pancreas injury. The rats were randomised into groups to receive (I) no therapy; (II) 50 lg/kg cerulein at 1 h intervals by four intraperitonally (i.p.) injections; (III) 50, 100 and 200 mg/kg CAR by one i.p. injection; and (IV) cerulein plus CAR after 2 h of cerulein administration. 12 h later, serum samples were obtained to assess pancreatic function, the lipase and amylase values. The oxidative stress markers were evaluated by changes in the amount of lipid peroxides measured as malondialdehyde (MDA) and changes in main tissue antioxidant enzyme levels including SOD, CAT and GSH-PX. Histopathological examination was performed using scoring systems. Additionally, oxidative DNA damage was determined by measuring the increases of 8-hydroxy-deoxyguanosine (8-OH-dG) formations. We found that the increasing doses of CAR decreased AP-induced MDA and 8-OH-dG levels. Moreover, the pancreas antioxidant enzyme activities were higher than that of the rats in the AP group when compared to the AP plus CAR group. In the treatment groups, the lipase and amylase were reduced. Besides, histopathological findings in the pancreatic tissue were alleviated (p \ 0.05). We suggest that CAR could be a safe and potent new drug candidate for treating AP through its antioxidative mechanism of action for the treatment of a wide range of disorders related to pancreas.

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“…Chemoprevention serves as an attractive alternative to control malignancy [7]. Several herbal drugs have been evaluated for their potential as liver protectant against DEN-induced hepatotoxicity in rats [8]. The recent approach to control liver cancer is chemoprevention, it is entirely prevented, slowed or reversed substantially by the administration of one or more nontoxic naturally occurring and/or synthetic agent, otherwise called as anticarcinogen [9].…”

Section: Introductionmentioning

confidence: 99%

Exploring the Potential Role of Chemopreventive Agent, Hesperetin Conjugated Pegylated Gold Nanoparticles in Diethylnitrosamine-Induced Hepatocellular Carcinoma in Male Wistar Albino Rats

et al. 2015

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Liver cancer is the fifth most common cancer and is still one of the leading causes of death world wide, due to food additives, alcohol, fungal toxins, air, toxic industrial chemicals, and water pollutants. Chemopreventive drugs play a potential role in liver cancer treatment. Obviously in the production of anticancer drugs, the factors like poor solubility, bioavailability, biocompatibility, limited chemical stability, large amount of dose etc., plays a major role. Against this backdrop, the idea of designing the chemopreventive nature of bio flavanoid hesperetin (HP) drug conjugated with pegylated gold nanoparticles to increasing the solubility, improve bioavailability and enhance the targeting capabilities of the drug during diethylnitrosamine (DEN) induced liver cancer in male wistar albino rats. The dose fixation studies and the toxicity of pure HP and HP conjugated gold nanoparticles (AumPEG (5000) -S-HP) were analysed. After concluded the dose fixation and toxicity studies the experimental design were segregated in six groups for the anticancer analysis of DEN induced HCC for 16 weeks. After the experimental period the body weight, relative liver weight, number of nodules and size of nodules, the levels of tumor markers like CEA, AFP and the level of lipid peroxidation, lipid hydroperoxides and the activities of antioxidant enzymes were assessed. The administration of DEN to rats resulted in increased relative liver weight and serum marker enzymes aspartate transaminase, alanine transaminase, alkaline phosphatase, lactate dehydrogenase, and gamma glutamyl transpeptidase. The levels of lipid peroxides elevated (in both serum and tissue) with subsequent decrease in the final body weight and tissue antioxidants like superoxide dismutase, catalase, reduced glutathione, glutathione peroxidise, and glutathione reductase. HP supplementation (20 mg/kg b.wt) significantly attenuated these alterations, thereby showing potent anticancer effect in liver cancer and the HP loaded gold nanoparticels (AumPEG (5000) -S-HP) treated animals shows the better treatment than the pure HP due to the solubility of drug, bioavailability and the target drug delivery of the biodegradable polymer. Histological observations were also carried out, which added supports to the chemopreventive action of the pure HP and HP loaded gold nanoparticles (Au-mPEG (5000) -S-HP) against DEN induction during liver cancer progression. These findings suggest that HP loaded gold nanoparticels (Au-mPEG (5000) -S-HP) shows better efficacy than the pure HP against lipid peroxidation, hepatic cell damage and protects the antioxidant system in DEN induced hepatocellular carcinogenesis.

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Potential preventive effect of carvacrol against diethylnitrosamine-induced hepatocellular carcinoma in rats

Cited by 176 publications

References 40 publications

The carvacrol ameliorates acute pancreatitis-induced liver injury via antioxidant response

The carvacrol ameliorates acute pancreatitis-induced liver injury via antioxidant response

Carvacrol modulates oxidative stress and decreases cell injury in pancreas of rats with acute pancreatitis

Exploring the Potential Role of Chemopreventive Agent, Hesperetin Conjugated Pegylated Gold Nanoparticles in Diethylnitrosamine-Induced Hepatocellular Carcinoma in Male Wistar Albino Rats

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