Unsaturated fatty acids as a co-therapeutic agents in cancer treatment.

Chemotherapy is standard treatments for many malignancies. However, in most cases, this method is not able to induce apoptosis and in many cases, with cancer recurrence, leads to patient death. There are several procedure to control and suppress malignant cells, but among these methods, administration of É·-3 fatty acids and É·-6 fatty due to their destructive effects on cancer cells is more prominent. Many clinical studies have shown beneficial effects of É·-3 and É·-6 fatty acids in cardiovascular disorders, asthma, rheumatoid arthritis, osteoporosis and in most cancers such as colon, breast, prostate and other malignancies. Studies showed that polyunsaturated fatty acids (PUFAs) have a toxic effect on cancer cells. However, the exact mechanism of how É·- fatty acids affect cancer cells is still unknown. In this review alternative issues of malignancies co-treatments agents such as PUFAs have been studied. Also, the latest known PUFAs mechanisms on malignancies have been described.

Hepatoprotective effects of Vaccinium arctostaphylos against CCl4-induced acute liver injury in rats.

BACKGROUND: This study was carried out to evaluate the antioxidant and hepatoprotective effects of Vaccinium arctostaphylos (V.a) methanolic extract on carbon tetrachloride (CCl4)-induced acute liver injury in Wistar rats. METHODS: Total phenolic and total flavonoid contents as well as antioxidant activity of V.a were determined. Extracts of V.a at doses of 200 and 400 mg/kg were administered by oral gavage to rats once per day for 7 days and then were given an intraperitoneal injection of 1 mL/kg CCl4 (1:1 in olive oil) for 3 consecutive days. Serum biochemical markers of liver injury, oxidative markers, as well as hydroxyproline (HP) content and histopathology of liver were evaluated. RESULTS: The obtained results showed that V.a had strong antioxidant activity. Treatment of rats with V.a blocked the CCl4-induced elevation of serum markers of liver function and enhanced albumin and total protein levels. The level of hepatic HP content was also reduced by the administration of V.a treatment. Histological examination of the liver section revealed that V.a prevented the occurrence of pathological changes in CCl4-treated rats. CONCLUSIONS: These findings suggested that V.a may be useful in the treatment and prevention of hepatic injury induced by CCl4.

Methanolic Extract of Dill Leaves Inhibits AGEs Formation and Shows Potential Hepatoprotective Effects in CCl4 Induced Liver Toxicity in Rat.

The research was aimed at evaluating the antiglycation, antioxidant, and hepatoprotective properties of methanolic extract of Anethum graveolens (dill). The antioxidant properties, photochemical characteristics, and antiglycation effects of dill extract were measured. Carbon tetrachloride-induced hepatotoxic rats were used to show the hepatoprotective activity of dill leaves. Different concentration of dill extract (0.032, 0.065, 0.125, 0.25, 0.5, and 1 mg/mL) showed potential antioxidant ability. The extract of dill leaves significantly reduced AGEs formation and also fructosamine and protein carbonyl levels in rats' liver. Thiol groups' oxidation, amyloid cross-ß, and protein fragmentation (P < 0.001) significantly reduced in treated rats. Liver damage markers significantly reduced in dill-treated animals (P < 0.05). Dill with potential antioxidant, antiglycation, and hepatoprotective effects can be suggested for treatment of diabetes complications.

Aqueous Extract of Anethum Graveolens L. has Potential Antioxidant and Antiglycation Effects.

The aim of this study was to assess the antiglycation and antioxidant properties of aqueous extract of Anethum graveolens (dill). In the in vivo and in vitro experiments, antioxidant properties, blood glucose, and AGEs formation were determined. Dill extract was given orally to healthy and diabetic rats. Our results illustrated that different concentrations of dill extract (0.125, 0.25, 0.5, and 1 mg/ml) have potential antiradical and antioxidant activity. Aqueous extract of dill significantly reduced AGEs formation and fructosamine levels, protein carbonyl and also thiol group's oxidation, amyloid cross-ß and fragmentation. After 2 months, blood glucose levels (P=0.006) and AGEs formation (P=0.003) significantly reduced in dill treated group compared with untreated diabetic animals. In conclusion, dill can be recommended as herbal medicine for the control and prevention of diabetic complications.

Effect of dill tablet (Anethum graveolens L) on antioxidant status and biochemical factors on carbon tetrachloride-induced liver damage on rat.

BACKGROUND: Liver damage induced by carbon tetrachloride (CCl4) has been presented as an experimental model for research in hepatoprotective effects of natural product. A commercial medicine prepared from Anethum graveolens L (dill) is being used as dill tablet (DT) as a hypolipidemic agent. This experiment aimed to investigate the protective effect of DT against hepatic damage. MATERIALS AND METHODS: Male Wistar rats were randomly divided into four groups (n = 6) as following for a 10 days experiments. (1) Normal animals; (2) normal animals +CCl4 1 ml/kg (1:1 of CCl4 in olive oil, by gastric tube); (3) CCl4 treated animals +100 mg DT/kg; (4) CCl4 treated animals +300 mg DT/kg. After 10 days of treatment, biochemical factors were measured; also antioxidant tests such as thiol group, malondialdehyde (MDA), total antioxidant capacity (TAC), and catalase (CAT) activity in the liver samples were carried out. RESULTS: In dill treated animals, a significant decrease in liver enzymes lactate dehydrogenase, alkaline phosphatase, aspartate transaminase, alanine transaminase, γ-glutamyl transferase, total bilirubin, direct bilirubin, as well as triglyceride, total cholesterol (P < 0.05) were observed. Total protein and albumin concentrations were significantly increased in dill treated groups (P < 0.05). Furthermore, treatment with dill declined liver cholesterol, triglyceride, MDA, and increased TAC and CAT activity compared with untreated group (P < 0.05). CONCLUSION: Dill displayed a potential hepatoprotective effect against CCl4-induced liver damage based on both biochemical markers and antioxidant status.

Effect of garlic on lipid profile and expression of LXR alpha in intestine and liver of hypercholesterolemic mice.

BACKGROUND: Garlic is one of the medicinal plants which has showed beneficial effects on atherosclerosis risk factors. The liver X receptor α (LXRα) is an important regulator of cholesterol, triglyceride and glucose homeostasis that belongs to the nuclear receptor superfamily. In this study we investigated the effect of garlic on lipid profile, glucose as well as LXRα expression in intestine and liver of mice. METHODS: Forty male N-Mary mice were randomly divided into 3 groups (n = 8): group1 received chow + 2% cholesterol + 0.5% cholic acid, group 2: chow + 4% (w/w) garlic extract + 2% cholesterol + 0.5% cholic acid, and group 3: chow only. After one month of treatment, mice were anesthetized, blood was collected from their heart, and the first 10 cm of the small intestine and liver were removed. Glucose was measured by a glucometer; other biochemical factors were measured by enzymatic methods. LXR expression was checked by RT-PCR and western blotting. RESULTS: Compared with hypercholesterolemic mice, treatment with garlic extract significantly decreased total cholesterol, low-density lipoprotein cholesterol (LDL-C), triglycerides, very low density lipoprotein-cholesterol (VLDL-C), atherogenic index, alanine aminotranferease (ALT) and aspartate aminotransferase (AST) (all of them P < 0.05). Change in HDL-C levels was not significant in garlic-extract treated animals compared with hypercholesterolemic group. LXR protein and mRNA in the intestine were increased in garlic-extract treated group compared with chow group (P < 0.05), while in the liver, only mRNA of LXR was increased in hypercholesterolemic control mice (P < 0.05). CONCLUSIONS: The present study demonstrated that garlic extract reduced LXRα expression in the liver and increased its expression in the intestine. These effects probably have an important role in reducing serum triglyceride and cholesterol.

Effect of garlic extract on some serum biochemical parameters and expression of npc1l1, abca1, abcg5 and abcg8 genes in the intestine of hypercholesterolemic mice.

Some compounds in the garlic inhibit cholesterol synthesis, resulting in lowering of serum cholesterol and triglycerides and increase in HDL level. However, the mechanism of this specific effect is not fully understood. In the small intestine, ATP-binding cassette transporters G5, G8 and A1 (ABCG5, ABCG8 and ABCA1), as well as Niemann-Pick C1 like 1 (NPC1L1) protein have important roles in cholesterol metabolism. In this study, we evaluated the beneficial effect of aqueous extract of garlic on lipid profile and also expression of npc1l1, abca1, abcg5 and abcg8 genes in the intestine of N-Marry mice fed a high cholesterol diet as a possible mechanism of garlic effect. Twenty-four mice were randomly divided into three groups: Group 1: hypercholesterolmic (received chow + 2% cholesterol + 0.5% cholic acid); Group 2: garlic (received chow + 4% (w/w) garlic extract + 2% cholesterol + 0.5% cholic acid); and Group 3: received chow only. After one month, mice were anesthetized and blood was collected from their heart. The jejunum was removed, washed with PBS and entrocytes were scraped and used for the experiments. Serum lipids were measured enzymatically and expression of mRNA levels for the above-mentioned proteins was determined by semi-quantitative RT-PCR. Garlic extract significantly reduced serum lipids (p < 0.05), compared with the hypercholesterolemic group. Expression of the intestinal npc1l1 was significantly decreased (p < 0.01) in the garlic group, compared with the chow group, while abcg5 (p < 0.01), abcg8 (p < 0.01) and abca1 (p < 0.05) expressions were significantly increased. In conclusion, this study reveals a possible mechanism for the beneficial effects of the garlic in lowering serum lipids by decreasing the intestinal lipid absorption and increasing excretion of cholesterol back into the intestinal lumen.