Attenuating effects of caffeic acid phenethyl ester and betaine on abamectin-induced hepatotoxicity and nephrotoxicity.

Abamectin (ABM) is a widely utilized potent anthelmintic and insecticidal agent. In this study, we investigated the protective effects of caffeic acid phenethyl ester (CAPE) and betaine (BET) against ABM-induced hepatotoxicity and nephrotoxicity in rats. Forty rats were divided into five groups, receiving either oral saline solution (normal control), oral ABM at a dose of 2 mg/kg BW (1/5 LD50), CAPE (10 µmol/kg BW intraperitoneally) followed by ABM, or BET supplementation at a dose of 250 mg/kg BW followed by ABM administration, while group V rats received a combination of i.p. CAPE and oral BET in the same doses before receiving ABM. Biochemical analysis showed that ABM administration significantly (p < 0.05) increased serum levels of aminotransferases, alkaline phosphatase, lactate dehydrogenase, and cholesterol, as well as serum creatinine and urea. Compared to the control group, ABM-intoxicated rats had significantly (p < 0.05) higher tissue concentrations of nitric oxide and malondialdehyde, as well as lower tissue glutathione concentration, total antioxidant capacity, and antioxidant enzymatic activity (glutathione peroxidase, superoxide dismutase, and catalase). Histopathological examination of hepatic and renal tissues of ABM-intoxicated rats showed acute inflammatory and necrotic changes. Pretreatment with CAPE and/or BET reversed the biochemical and histopathological alterations of ABM on the liver and kidneys. Therefore, CAPE and BET (alone or in combination) could be promising protective agents against ABM-induced hepatotoxicity and nephrotoxicity. Future studies should confirm our findings and evaluate the other molecular effects are involved in the combination chemoprotection of CAPE and BET.

Peppermint essential oil alleviates hyperglycemia caused by streptozotocin- nicotinamide-induced type 2 diabetes in rats.

The prevalence of diabetes mellitus is steadily growing throughout the world. Traditional medicine has an excellent potential in the treatment of diabetes mellitus. The present study was undertaken to evaluate the potential antidiabetic effect of peppermint essential oil (PEO) on streptozotocin (STZ) and nicotinamide induced diabetic rats. Diabetes was induced in rats fasting overnight by the intraperitoneal administration of nicotinamide followed by a single dose of STZ. After 72h, two groups of diabetic rats were treated with different doses of PEO (40 and 80mg/kg BW) respectively and one group was treated with the standard hypoglycemic agent glibenclamide. The levels of blood glucose, serum insulin, and C-peptide were estimated. The markers of oxidative stress were quantified. The samples from liver and pancreas were collected for histological evaluation. Immunohistochemical tests were carried out to determine the expression of Bcl-2 and insulin in the liver and pancreas, respectively. After the treatment with PEO, it was observed that anemia resulting from diabetes was rectified, the counts of leukocytes and platelets, which decreased during diabetes, were increased, the levels of blood glucose were decreased and those of serum insulin and C-peptide were increased. The administration of PEO also enhanced the antioxidant status in the treated rats. The histological analysis revealed regeneration of the hepatic and pancreatic tissues and the extent of degenerative changes were reduced. The immunohistochemical examination revealed upregulation in the expression of Bcl-2 and insulin. These findings demonstrated the potential antidiabetic capability of PEO.

Ameliorative effect of parsley oil on cisplatin-induced hepato-cardiotoxicity: A biochemical, histopathological, and immunohistochemical study.

Cisplatin (cis-diamminedichloroplatinum, CDDP) is an effective DNA alkylating agent used in the treatment of different types of tumors; however, its clinical use is associated with hepato-cardiotoxicity. The current study was designed to assess the potential protective effect of parsley oil (PO) against CDDP-induced hepato-cardiotoxicity. For this purpose, 25 adult male rats were assigned into five groups, each containing five animals. Group I (control) was administered saline solution. Group II was administered PO at a dosage of 0.42ml/kg BW. Group III were administered CDDP at a dosage of 5mg/kg BW. Group IV was administered PO in addition to CDDP. Group V was administered saline solution in addition to CDDP, after which they were administered PO for five days. Oral administration of either saline solution or PO was performed each day for 10days, while administration of CDDP was via a single intraperitoneal injection five days following the commencement of the experiment. The recorded results revealed that CDDP induced obvious hepatic and cardiac injuries that were indicated by biochemical, histopathological, and immunohistochemical alterations, including elevation of serum hepatic and cardiac injury markers as well as proinflammatory cytokines. Moreover, CDDP induced an increase in the level of hepatic and cardiac injury biomarkers, decreases in the activities of antioxidant enzymes, a decrease in GSH concentration, and an increase in MDA concentration. CDDP also induced histopathological hepatocellular and myocardial changes, and overexpression of p53 and COX-2 in hepatic and cardiac tissues. Administration of PO either as a preventative medicine or as treatment significantly improved all the observed deleterious effects induced by CDDP in rat liver and heart. Thus, it may be concluded that PO, with its antioxidant, anti-inflammatory, and antiapoptotic activities, can potentially be used in the treatment of CDDP-induced hepatic and cardiac injuries.

Ameliorative effect of flaxseed oil against thiacloprid-induced toxicity in rats: hematological, biochemical, and histopathological study.

The present study was carried out to evaluate the hematological, biochemical, and histopathological changes due to thiacloprid toxicity, and the potential protective role of flaxseed oil in male Wistar albino rats. Subacute thiacloprid intoxication induced a significant increase in RBCs, Hb, PCV, and WBCs count, and bone marrow micronucleus (MN) formation. Moreover, there was a significant increase in serum biochemical parameters related to hepatic injury: alanine aminotransferase (ALT) and alkaline phosphatase (ALP). Serum total protein and albumin levels were significantly reduced. Thiacloprid increases tumor necrosis factor-alpha (TNF-α) and interleukine-2(IL-2). There was a significant decrease in glutathione-S-transferase, while the lipid peroxidation (MDA) and cytochrome P450 activity were significantly increased. Flaxseed oil coadministration partially retrieved the changes in all studied parameters. Thiacloprid induced histopathological liver damage, which was minimized as a result of flaxseed oil treatment. In general, it was concluded that, flaxseed oil able to protect against thiacloprid-induced hepatoxicity.