Antidepressant-like effect of aqueous extract of Channa striatus fillet in mice models of depression

Abstract. -Background and Objectives: Channa (C.) striatus (Malay-Haruan), is a fresh water snakehead fish, consumed as a rejuvenating diet in post-parturition period in local Malay population. The aqueous extract of C. striatus fillet (AECSF) was reported to act through serotonergic receptor system in a previous study. There is no scientific report on neuropharmacological effects of C. striatus. Based on these data, the antidepressant-like effect of C. striatus was evaluated in mice models of depression. Materials and Methods: AECSF was prepared by steaming the fillets as described previously. Antidepressant activity was studied in male ICR mice using forced swimming test (FST) and tail suspension test (TST). Open-field test was used to evaluate any psychomotor stimulant activity. AECSF was administered intraperitoneally at the concentrations of 30%, 40% and 50% w/v at the dosage of 10 ml/kg. Amitriptyline (10 mg/kg) was used as positive control. Results: All the three concentrations of AECSF (30%, 40% and 50% w/v) significantly reduced the immobility time (p < 0.001) in FST and TST. All the three concentrations of AECSF (30%, 40% and 50% w/v) significantly (p < 0.001) reduced locomotor activity in a dose-dependent manner in open-field test. Conclusions: AECSF produced significant reduction of immobility time in both FST and TST. Amitriptyline produced a significant reduction of immobility time in both FST and TST similar to previous findings. The AECSF produced a dosedependent decrease in locomotor activity in the open-field test. This hypolocomotion effect indicated the absence of any psychomotor stimulant activity thereby supporting the antidepressantlike effect of the AECSF. The pharmacological mechanisms of the observed antidepressant-like effect and hypolocomotion effect are not understood from our study. Hence, further studies are required

Improving the lipid profile in hypercholesterolemia-induced rabbit by supplementation of germinated brown rice.

It is imperative that there be a diet designed specifically to improve lipid profile in order to impede the progress of atherosclerosis. Because rice is a staple food in Asia, it will be chosen as the diet of interest. This study sets out to discover whether consumption of different processed rice diets may result in a change of the lipid profile. The experiment was done on male New Zealand white rabbits after 10 weeks of treatment with diet containing 0.5% cholesterol. The experimental diets include white rice (WR), brown rice (BR), and germinated brown rice (GBR). Among them, rabbits fed a GBR diet demonstrated significantly lower levels of total cholesterol (TC), low-density lipoprotein (LDL), LDL/HDL, and atherogenic index (AI) and a higher level of high-density lipoprotein (HDL). Results from atherosclerotic plaque assessment further support the findings. The level of malondialdehyde (MDA), which acts as an indicator for oxidative stress, was also reduced by GBR diet. The positive change in lipid profile in the rabbits fed GBR appeared to correspond with the higher amounts of γ-oryzanol, tocopherol, and monounsaturated fatty acid (MUFA) content

A novel ubiquitin ligase is deficient in Fanconi anemia.

Fanconi anemia is a recessively inherited disease characterized by congenital defects, bone marrow failure and cancer susceptibility. Cells from individuals with Fanconi anemia are highly sensitive to DNA-crosslinking drugs, such as mitomycin C (MMC). Fanconi anemia proteins function in a DNA damage response pathway involving breast cancer susceptibility gene products, BRCA1 and BRCA2 (refs. 1,2). A key step in this pathway is monoubiquitination of FANCD2, resulting in the redistribution of FANCD2 to nuclear foci containing BRCA1 (ref. 3). The underlying mechanism is unclear because the five Fanconi anemia proteins known to be required for this ubiquitination have no recognizable ubiquitin ligase motifs. Here we report a new component of a Fanconi anemia protein complex, called PHF9, which possesses E3 ubiquitin ligase activity in vitro and is essential for FANCD2 monoubiquitination in vivo. Because PHF9 is defective in a cell line derived from an individual with Fanconi anemia, we conclude that PHF9 (also called FANCL) represents a novel Fanconi anemia complementation group (FA-L). Our data suggest that PHF9 has a crucial role in the Fanconi anemia pathway as the likely catalytic subunit required for monoubiquitination of FANCD2