histopathology

Objective: The present investigation aimed to study the protective effects of aqueous extract of Moringa olifera (MOR) leaf powder against the side effects of Adriamycin ADR (an anthracycline antibiotic, used in tumor therapy) on the hematological and biochemical functions of male albino rats. Animal's studies and drug treatment: 48 male albino rats weighing 180 ± 10.0 gm were taken and divided into six groups each one consists of 8 male rats. The 1st group was fed adlibitum with saline without any treatment so called control. The 2nd group received MOR leaf powder aqueous extract orally with a daily dose 144 mg/Kg body weight for 30 days. The 3rd one is ADR group where the animals were injected intraperitoneal (IP) from the first day in six equal injections of ADR (each containing 3 mg/kg b.wt.) over a period of two weeks (total cumulative dosage of 18 mg/kg body weight). The 4th is ADR then MOR post-treated group where animals administered the same six injections of ADR dose of thereafter they were given the aqueous MOR leaf powder extract orally from day 20. The 5th is ADR/MOR treated group where animals received six equal injections of ADR over a period of 19 days and given concomitant orally a daily dose of MOR leaf powder aqueous extract of 144 mg/kg of body weight for 30 days. The 6th group was (MOR pretreated then ADR group) where animals given orally once daily dose of MOR aqueous extract of 144 mg/Kg b.wt for 30 days and at the 11th day received the six equal injections of ADR over a period of 19 days. The results revealed loss in body weight, an increase in mortality rate, disturbances in hematological parameters, liver and kidney functions of rats treated with adriamycin. In contrast, the Moringa improves the studied parameters to levels more or less similar to that of control group. Conclusions: This study revealed that Moringa may ameliorate the effect of ADR especially in the group that pretreated with Moringa before Adriamycin treatment.

Background: Sorafenib (Nexavar) is an oral inhibitor of multi-kinase proteins approved in 2005 for treatment of metastatic advanced hepatocellular carcinoma. It causes many metabolic side effects, including diarrhea, hypertension, hand-foot skin reaction, and fatigue. This study aims to detect the histopathological, histochemical and DNA contents changes of the rat's liver under Nexavar treatment. Methods: The rats were divided into 3 groups. • Group 1: Served as control (rats were orally administrated with ml of normal saline for a month. • Group 2: Rats of this group were treated with the multikinase inhibitor Sorafenib (60 mg/kg body weight/day) for 15 days by gavage. • Group 3: Rats of this group were treated with the multikinase inhibitor Sorafenib (60 mg/kg body weight/day) for 30 days by gavage. Animals were sacrificed and specimens from the liver were processed for histopathological, histochemical; by estimation of total carbohydrates and total protein contents; and cytological studies by estimation of DNA contents at the different stages of the cell cycle by the flow cytometer analysis. Results: In treated animals, there were histopathological and histochemical alterations, as a destruction of the normal hepatic architecture, swollen hepatocytes with vacuolar degenerated cytoplasm. Some hepatocytes showed mild to severe signs of injury such as swelling of their nuclei. Karyolysis of other hepatocytes are encountered. Severe reduction in the glycogen and proteins contents of the hepatocytes was observed by using PAS and bromophenol blue staining techniques. Moreover, the results showed that Nexavar causes apoptosis by 15.41% and 13.72% in both groups 2 and 3, respectively. Liver genotoxicity induced by Nexavar for 15 and 30 days decreases the G1 cells constitute to 5.08% and 6.50% and increases the S-phase cells constitute to 19.17% and 20.28%, respectively. Moreover, the G2 cells increases to 2.32% and 2.45, about half of the last amount is aneuploidy cells. Conclusion: Nexavar treatment showed mild to moderate hepatotoxic effects and induces many histological, histochemical and cytological changes causing liver damage.