The Protective Role of Urtica dioica Seed Extract Against Azoxymethane-Induced Colon Carcinogenesis in Rats.

The aim of this study was to investigate the protective role of Urtica dioica seed (UDS) extract against azoxymethane (AOM)-induced colon carcinogenesis in rats. Thirty-two male Wistar albino rats were divided into four groups: Control, AOM, AOM + UDS, and UDS. The AOM and AOM + UDS groups were induced by AOM (15 mg/kg body weight) subcutaneously once a week for 10 weeks. AOM + UDS and UDS groups additionally received fed with pellets included 30 ml/kg UDS extract. At the end of the trial, blood and colon tissue samples were taken from the rats following necropsy. The gross and histopathological findings revealed that the administration of UDS extract significantly decreased lesions including aberrant cript foci, adenoma, and adenocarcinoma formation both numerically and dimensionally. Immunohistochemically, slight CEA and COX-2, strong Caspase-3 immune-expressions were detected in the group AOM + UDS compared to AOM group. Biochemical examinations indicated that a markedly increase in the malondialdehyde and fluctuated antioxidant defense system constituents levels such as reduced glutathione, glutathione s-transferase, glutathione peroxidase, superoxide dismutase were restored in AOM + UDS group. These results reveal that the UDS may act as a chemopreventive dietary agent, inducing apoptosis, resulting in a significant reduction of colon carcinogenesis.

Reduction of hepatorenal and pancreatic damage by Ferula elaeochytris extract in STZ induced diabetic rats.

The therapeutic potential and antioxidant capacity of Ferula elaeochytris extract (FE) in the liver, kidney and pancreas of rats with diabetes induced by streptozotocin (STZ) was assessed using biochemistry, histopathology and immunohistochemistry. Forty adult Wistar albino male rats were divided randomly into five groups of eight rats each. The normal control (NC) group was untreated. The diabetes control (DC) group was treated with STZ to induce diabetes. The diabetes + acarbose group (DAC) was treated with STZ, then with acarbose daily for 28 days. The diabetes + FE (DFE) group was treated with STZ, then FE daily for 28 days. DC rats had inflammatory cell infiltration, hydropic degeneration and necrosis, whereas the DFE rats exhibited nearly normal histology. Insulin immunostaining in the pancreatic beta cells was decreased in the DC group compared to the NC group, whereas the DFE group was similar to the NC group. Many serum biomarkers of damage to liver, kidneys or pancreas were elevated in the DC group compared to the NC group; these biomarkers were decreased in the DFE group. The DC group exhibited increased malondialdehyde levels and decreased levels of the antioxidant defense system constituents compared to the NC group. The level of biomarkers the DFE group was close to the NC group. FE exhibited a protective effect against tissue damage owing to its antioxidant activities and to its ability to effect regeneration of ß-cells in STZ induced diabetic rats.

Chemopreventive efficacy of juniper berry oil (Juniperus communis L.) on azoxymethane-induced colon carcinogenesis in rat.

The aim of this study was to investigate the chemopreventive effects of juniper berry (JB) oil on azoxymethane (AOM)-induced colon cancer in rats. Thirty-two male Wistar albino rats were allocated into four groups: Control, AOM, AOM + JB, and JB groups. Whereas the control group was fed with standard pellet feed, the AOM and AOM + JB groups were administered of AOM (15 mg/kg body weight) subcutaneously once every 2 weeks for 10 weeks. AOM + JB and JB groups additionally received JB oil (100 µl/kg) orally. At the end of the 16-week experimental period, blood and tissue samples were obtained from the rats following necropsy. The macroscopic findings showed that the application of JB oil significantly decreased adenoma and adenocarcinoma formation both numerically and dimensionally. Immunohistochemically, CEA, COX-2, and Ki-67 immune-expressions decreased, and the immune-expression of caspase-3 increased in AOM + JB treated rats. Additionally, JB oil supplementation ameliorated antioxidant defense systems and lipid peroxidation within the colon tissue of AOM + JB treated rats. These results reveal that the JB oil acted as a chemopreventive dietary agent, inhibiting cell proliferation and COX-2 expression and inducing apoptosis, resulting in a significant reduction in colon tumor formation.

Protective effects of silymarin on methotrexate-induced damages in rat testes

Abstract The present study aimed to investigate the protective effects of silymarin (SMN), an antioxidant, on methotrexate (MTX)-induced damage in rat testes. Thirty-two Wistar albino rats were divided into four groups (n = 8): control, MTX (20 mg/kg, i.p. on days 1 and 5), SMN (200 mg/kg, orally), and MTX + SMN (20 mg/kg, i.p. on days 1 and 5 and SMN 200 mg/kg orally) groups. At the end of the 6-week trial period, histopathological, immunohistochemical, biochemical, and spermatological analyses were performed on testes tissues. Histopathologically, MTX-induced damage, including depletion of germ cell and loos of spermatozoa, was significantly improved with SMN treatment. Immunohistochemically, the immunoreactivity of glutathione peroxidase 1 (GPx1) and manganese superoxide dismutase 2 (SOD2) were detected more intensely in the MTX + SMN group than in the MTX group. Biochemical examinations revealed that SMN supplementation decreased the lipid peroxidation and increased enzymatic antioxidants in the SMN-treated rats. Spermatologically, significant differences were found in the density, motility, dead-to-live sperm ratio, and abnormal sperm rate in the MTX + SMN group compared to the MTX group. In conclusion, SMN seems to have protective effects as an antioxidant against MTX-induced damage in rat testes.

Histopathological and biochemical investigations of protective role of honey in rats with experimental aflatoxicosis.

BACKGROUND: Natural honey (honey) is considered as a part of traditional medicine all over the world. It has both antimicrobial and antioxidant properties, useful in stimulation of wounds and burns healing and gastric ulcers treatment. The aim of this study, for the first time, was to investigate the antioxidant properties and protective role of honey against carcinogen chemical aflatoxin (AF) exposure in rats, which were evaluated by histopathological changes in liver and kidney, measuring level of serum marker enzymes [aspartate aminotransferase (AST), alanin aminotransferase (ALT), gamma glutamil transpeptidase (GGT)], antioxidant defense systems [Reduced glutathione (GSH), glutathione reductase (GR), superoxide dismutase (SOD), glutathione-S-transferase (GST) and catalase (CAT)], and lipid peroxidation content in liver, erythrocyte, brain, kidney, heart and lungs. METHODS: Eighteen healthy Sprague-Dawley rats were randomly allocated into three experimental groups: A (Control), B (AF-treated) and C (AF + honey-treated). While rats in group A were fed with a diet without AF, B, and C groups received 25 µg of AF/rat/day, where C group additionally received 1 mL/kg of honey by gavage for 90 days. RESULTS: At the end of the 90-day experimental period, we found that the honey supplementation decreased the lipid peroxidation and the levels of enzyme associated with liver damage, increased enzymatic and non-enzymatic antioxidants in the AF + honey-treated rats. Hepatoprotective and nephroprotective effects of honey is further substantiated by showing almost normal histological architecture in AF + honey-treated group, compared to degenerative changes in the liver and kidney of AF-treated rats. Additionally, honey supplementation ameliorated antioxidant defens systems and lipid peroxidation in content in other tissues of AF + honey treated rats. CONCLUSION: The present study indicates that honey has a hepatoprotective and nephroprotective effect in rats with experimental aflatoxicosis due to its antioxidant activity.

Effects of Urtica dioica L. seed on lipid peroxidation, antioxidants and liver pathology in aflatoxin-induced tissue injury in rats.

This study was carried out to investigate the hepatoprotective and antioxidant properties of Urtica dioica L. seeds (UDS) extract against aflatoxin (AF)-exposure in rats. The preventive potential and antioxidant capacity of the plant's extract was evaluated by liver histopathological changes, measuring serum marker enzymes, antioxidant defense systems and lipid peroxidation (Malondialdehyde, MDA) content in some tissues of rats. Eighteen rats were randomly divided into one of three experimental groups: control, AF-treated group and AF+UDS-treated group. Rats in control group were fed with a diet without AF. Rats in AF-treated group and AF+UDS-treated group received approximately 25 microgr of AF/rat/day. AF+UDS groups also received 2 mL of UDS oils/rat/day by gavage for 90 days. Administration of UDS extract restored the AF-induced imbalance between MDA and antioxidant system towards near normal particularly in liver. Hepatoprotection by UDS is further substantiated by the almost normal histologic findings in AF+UDS-treated group as against degenerative changes in the AF-treated rats. It is concluded that UDS has a hepatoprotective effect in rats with aflatoxicosis, probably acting by promoting the antioxidative defense systems.

Partial regeneration/proliferation of the beta-cells in the islets of Langerhans by Nigella sativa L. in streptozotocin-induced diabetic rats.

This experiment was carried out to investigate the effect of N. sativa L. on histopathology of pancreatic beta-cells, and blood insulin and glucose concentrations in streptozotocin-induced diabetic rats. Fifty male Wistar rats (200-250 g) were divided into two experimental groups (diabetics with no treatment and diabetics with N. sativa L. treatment), each containing twenty-five rats. Diabetes was induced in both groups by a single intraperitoneal injection of streptozotocin (STZ) (50 mg/kg). The experimental animals in both groups became diabetic within 24 hours after the administration of STZ. The rats in N. sativa L.-treated group were given the daily intraperitoneal injection of 0.20 ml/kg of N. sativa L. volatile oil for 30 days starting the day after STZ injection. Control rats received only the same amount of normal saline solution. The rats in both groups received the last injection 24 hours before the sacrification and 5 randomly-selected rats in each group were sacrificed before, and the 1, 10, 20 and 30 days after the STZ injection to collect blood and pancreatic tissue samples. The N. sativa L. treatment caused a decrease in the elevated serum glucose, an increase in the lowered serum insulin concentrations and partial regeneration/ proliferation of pancreatic beta-cells in STZ-induced diabetic rats with the elapse of the experiment. It is concluded that the hypoglycaemic action of N. sativa L. could be partly due to amelioration in the beta-cells of pancreatic islets causing an increase in insulin secretion. More studies are needed to demonstrate the exact mechanism of action of N. sativa L. on ameliorated blood glucose concentration in STZ-induced diabetes.