Periasamy Srinivasan

Anti-peroxidative and anti-hyperlipidemic nature of Ulva lactuca crude polysaccharide on D-Galactosamine induced hepatitis in rats

To find whether pretreatment of Ulva lactuca polysaccharide (ULP) extract could be effective against D-Galactosamine (500 mg/kg body weight, i.p.) induced anomaly in rat. Serum total cholesterol (TC), triglycerides (TG), free fatty acid (FFA), phospholipids (PL), high density lipoprotein (HDL), low density lipoprotein (LDL), very low density lipoprotein (VLDL), tissue lipoperoxides (LPO), hepatic protein thiols, non-enzymatic anti-oxidants glutathione (GSH) and vitamins (E and C) were examined using spectrophotometer. The ultra structural changes of liver during D-Galactosamine and protection offered by ULP were examined by electron microscopy. Seaweed histology and chemical composition of polysaccharides in seaweed were examined. Alcian blue staining showed the presence of sulphated polysaccharide with total sugar (65.4%), sulphate (17.4%), and uronic acid (17.2%) content. D-Galactosamine intoxicated rats showed significant (p<0.01) liver damage with acute aberration in serum lipid profile, hepatic protein thiols and tissue non-enzymatic anti-oxidants. Assorted deposits of lipid droplets and abnormal appearance of mitochondria was observed in electron microscopy study. Rats pretreated with ULP (30 mg/kg body weight/day/for 21 days) showed a significant inhibition (p<0.05) against abnormality induced by d-Galactosamine. U.lactuca exhibit anti-peroxidative and anti-hyperlipidemic property.

Comparison of hypolipidemic activity of synthetic gallic acid–linoleic acid ester with mixture of gallic acid and linoleic acid, gallic acid, and linoleic acid on high-fat diet induced obesity in C57BL/6 Cr Slc mice

Hyperlipidemia is the major risk factors of heart disease such as atherosclerosis, stroke, and death. In the present study, we studied the effect of gallic acid (GA), linoleic acid (LA), mixture of GA and LA (MGL), and chemically synthesized gallic acid-linoleic acid ester (octadeca-9,12-dienyl-3,4,5-trihydroxybenzoate, GLE) on the ability to ameliorate hyperlipidemia in C57BL/6 mice fed a high-fat diet (HFD). GLE, GA, LA, and MGL were mixed with HFD and the composition of the test compounds were 1% of the diet for 7 weeks. After 7 weeks, the average body weight of ND and GLE groups was lower than that of HFD group (P<0.05). The liver weight of mice decreased (P<0.05) in all treatment groups relative to HFD fed group. The plasma lipids such as triglyceride and LDL-cholesterol were found to be decreased (P<0.05) in GLE, GA, LA, and MGL fed mice when compared to that of HFD fed mice. But high-density lipoprotein (HDL) cholesterol increased (P<0.05) in HFD and GLE fed mice when compared to that of ND fed mice. The hepatic accumulation of fat droplets of GA, LA, GLE, and MGL group showed considerably lower than that of HFD group. Adipose histology showed that GLE supplementation was found to be more effective in decreasing the size of adipocyte relative to those of other treatment groups. In conclusion, the supplementation of synthetic GLE from gallic acid and linoleic acid ester may have a potential hypolipidemic effect on mice fed high-fat diet. Further studies are required to prove GLE as a hypolipidemic agent.

Structural and antioxidant properties of gamma irradiated hyaluronic acid.

Hyaluronic acid (Hyaluronan, HA) was depolymerised by gamma irradiation and its structural changes and antioxidant activities were investigated. The structural changes of gamma irradiated HA were studied by gel-permeation chromatography (GPC), viscosity, pH, Hunter colour measurement, UV spectrophotometry, and FT-IR spectroscopy. The results demonstrated that gamma irradiation decreased molecular weight size, viscosity and pH of the hyaluronic acid and its colour turned to intense yellow. UV spectra of the irradiated HA showed a change at 265nm, which indicates the formation of double bonds. Differences in the height and shape of certain absorption bonds of FT-IR spectra in the range 1700-1750cm(-1) were also observed, which is associated with the formation of carboxylic acid. From these structural changes of the HA, gamma irradiation may have a role in the formation of pyrancarboxylic acid rings. DPPH radical scavenging ability and the reducing power of gamma irradiated HA were significantly higher than that of non-irradiated HA. However, non-irradiated and irradiated HA did not show significant differences in the Rancimat test.

Immunomodulatory activity of fucoidan against aspirin-induced gastric mucosal damage in rats

Gastric ulcers and related complications associated with the use of non-steroidal anti-inflammatory drugs (NSAIDs), such as aspirin, represent a major global health problem. In the present study, we investigate the immunological activity of fucoidan against aspirin-induced gastric mucosal damage in rats. Thirty-six rats were randomly divided into the following, normal (Carboxy methyl cellulose 0.05 %), aspirin (Asp-400mg/kg) treated, fucoidan alone (Fu-0.02 g/kg, daily for 14 days) and Fu+Asp. Cytokines, total nitrite and nitrate (NOx) analysis and tissue localization of Cyclooxygenase 1, 2 and epidermal growth factor receptor (EGFR) were done using Elisa and immunohistochemistry respectively. Histopathology of gastric tissue, collagen deposition was performed using Hematoxylin and Eosin and Massons trichrome were performed. Treatment of rats with a single dose of aspirin (400mg/kg, orally) led to significant alterations in the levels of total nitrite and nitrate (NOx), interleukins (IL-4, 6, 10, 12), tumor necrosis factor (TNF-α), and interferon gamma (IFN-γ). Notably, collagen deposition in glandular tissue and localization of cyclooxygenase 1, 2, and epidermal growth factor were considerably affected in aspirin-treated rats. These severities were prevented to a significant extent in rats pretreated with fucoidan (0.02 g/kg/day for two weeks orally). Our findings collectively indicate that the gastro-protective effect of fucoidan against aspirin-induced ulceration in rats is mediated through its immunomodulatory properties.

γ-Irradiation Improves the Color and Antioxidant Properties of Chaga Mushroom (Inonotus obliquus) Extract

The objective of this study was to evaluate the effect of ionizing radiation on color and antioxidative properties of Chaga mushroom (Inonotus obliquus) extract (CME). CME (10 mg/mL) was gamma-irradiated at 0, 3, 5, 7, and 10 kGy, and color, antioxidant activity, and total phenolic compound levels were then determined. The lightness and yellowness were increased (P < .05), and the redness was decreased (P < .05), as irradiation dose increased. The antioxidant parameters such as the 2-diphenyl-1-picrylhydrazyl, superoxide, and hydroxyl radical scavenging activities, ferric reducing/antioxidant power, and inhibition of lipid peroxidation increased as the irradiation dose increased. Also, the total phenolic compound levels of CME were increased (P < .05) by gamma-irradiation. These results suggest that gamma-irradiation could be considered a means for improving the antioxidant properties and the color of CME.

Sesamol attenuates oxidative stress–mediated experimental acute pancreatitis in rats

Acute pancreatitis is a potentially fatal disease with no known cure. The initial events in acute pancreatitis may occur within the acinar cells. We examined the effect of sesamol on (i) a cerulein-induced pancreatic acinar cancer cell line, AR42J, and (ii) cerulein-induced experimental acute pancreatitis in rats. Sesamol inhibited amylase activity and increased cell survival. It also inhibited medium lipid peroxidation and 8-hydroxydeoxyguanosine in AR42J cells compared with the cerulein-alone groups. In addition, in cerulein-treated rats, sesamol inhibited serum amylase and lipase levels, pancreatic edema, and lipid peroxidation, but it increased pancreatic glutathione and nitric oxide levels. Thus, we hypothesize that sesamol attenuates cerulein-induced experimental acute pancreatitis by inhibiting the pancreatic acinar cell death associated with oxidative stress in rats.

Effect of gamma irradiated hyaluronic acid on acetaminophen induced acute hepatotoxicity

The hepatoprotective efficacy of irradiated hyaluronic acid (HA) on acetaminophen (APAP) induced acute hepatotoxicity was investigated. BALB/c mice (4-6 weeks of age) were pretreated with unirradiated HA (UIHA), 5 and 50 kGy gamma irradiated HA (GIHA) for 14 days and were dosed APAP (500 mg/kg b.wt). After 9h of APAP dosing animals were euthanized. The degree of acute hepatotoxicity was measured by aspartate aminotransferase (AST) and alanine aminotransferase (ALT). The expression of interferon-gamma (IFN-gamma) in serum and alpha-and mu-class of gluthathione-S-transferase (GSTs), CYP 2E1 class of cytochrome monooxygenase and glutathione (GSH) in liver were quantified. Histological evaluation was done by Hematoxiylin and Eiosin staining, Periodic acid schiffs staining, Manson trichrome staining and histological scorings were done. The degree of acute hepatotoxicity was markedly lower in UIHA and 5 kGy than in 50 kGy GIHA pretreated group and there was negligible difference between 5 and 50 kGy GIHA pretreated group. The expression of interferon-gamma (IFN-gamma) was significantly (P<0.05) suppressed in 5 and 50 kGy GIHA pretreated group. Histological scorings showed a significant protection of liver in UIHA and 5 kGy GIHA pretreated mice. Expression of alpha class GSTs was significantly increased in 5 and 50 kGy GIHA pretreated group. To conclude suppression of IFN-gamma and increase in alpha-class GSTs expression may exert a protective role in acute hepatotoxicity of APAP and 5 kGy GIHA showed comparable protective effect to that of UIHA.

Comparative potential therapeutic effect of sesame oil and peanut oil against acute monocrotaline (Crotalaria) poisoning in a rat model.

BACKGROUND Many Crotalaria plant species contain hepatotoxic pyrrolizidine alkaloids (such as monocrotaline) that can cause acute and chronic poisoning in cattle and other animals. HYPOTHESIS Peanut oil, atropine sulfate, and antidiarrheal agents are used to treat acute monocrotaline poisoning. The effect of sesame on acute monocrotaline poisoning has never been investigated. ANIMALS Fifty male Sprague-Dawley rats were used for toxicity studies. METHODS Experiment 1: Group I, control. Groups II-IV were given monocrotaline (205.2 mg/kg) and euthanized 6, 12, and 24 hours later. Experiment 2: Group I, control. Group II monocrotaline alone (205.2 mg/kg). Groups III-VI were given monocrotaline (205.2 mg/kg) and 1 hour later, Groups III and IV were given sesame oil (1 and 2 mL/kg) and Groups V and VI were given peanut oil (1 and 2 mL/kg). RESULTS Monocrotaline significantly decreased (P < .05) serum amylase activity, but, over time, increased (P < .05) pancreatic and lung injury. AST and ALT activity and liver injury peaked at 24 hours. Sesame oil and peanut oil (P < .05) inhibited the changes in all tested parameters in acute monocrotaline poisoning. Although peanut oil inhibited acute monocrotaline poisoning, it induced steatosis, but sesame oil did not. CONCLUSION AND CLINICAL IMPORTANCE We hypothesize that early pancreatic and lung injury and late liver injury contribute to acute monocrotaline poisoning and that sesame oil is more efficacious than peanut oil against acute monocrotaline poisoning in rats. However, additional studies are needed to confirm that these oils have the same effects in cattle and other animals.

Ostensibly ineffectual doses of cadmium and lipopolysaccharide causes liver damage in rats

Various hepatotoxicants co-treated with lipopolysaccharide (LPS) have the potential to cause severe hepatic damage. Whether co-treatment with ostensibly ineffectual (without effect on customary clinical liver function tests, such as aspartate aminotransferase and alanine aminotransferase) doses of cadmium (Cd) and LPS cause liver damage is still unknown. We examined the effects of treating ostensibly ineffectual doses of Cd and LPS on liver dysfunction as well as on liver histopathology. We injected rats with saline only, Cd only, LPS only, or a single ostensibly ineffectual dose of Cd (100 μg/kg body weight) plus LPS (0.1 mg/kg body weight). After 6 h, the rats were killed and their liver damage was assessed. Co-treated with ostensibly ineffectual doses of Cd and LPS had higher levels of aspartate aminotransferase and alanine aminotransferase, hepatic lipid peroxidation, peroxynitrite, nitrite, and interleukin-1β (IL-1β), but lower levels of hepatic metallothionein (MT) than did that treated with saline only, Cd only, and LPS only. Histopathological analysis of Cd only and LPS only showed apparent liver damage, but Cd plus LPS showed marked hepatic damage. We conclude that co-treating the rats with ostensibly ineffectual doses of Cd and LPS is hepatotoxic. Cd promotes LPS-initiated oxidative-stress-associated liver damage by increasing IL-1β and decreasing MT levels in rats.