Chronic administration of rosa canina hydro-alcoholic extract attenuates depressive-like behavior and recognition memory impairment in diabetic mice: a possible role of oxidative stress

Objective: This study was designed to evaluate whether chronic Rosa canina [RC] extract administration could improve recognition memory and depressive-like behavior in diabetic mice

Materials and Methods: Seventy-five male albino mice [25-30 g] were randomly divided into 5 groups [15 in each group]

A single intraperitoneal injection of 200 nng/ kg streptozotocin [STZ] was administered to the mice to induce diabetes

The control group received normal saline, and the diabetic groups received normal saline or 50, 250, and 500 mg/kg of RC extract for 28 days

The mice were weighed each week

Recognition memory and depressive-like behavior were assessed using forced swimming and novel object recognition [NOR] tests, respectively. Malondi-aldehyde [MDA] levels and total antioxidant capacity [TAG]were measured in the mouse brain homogenate to evaluate oxidative stress. Statistical analysis was conducted using SPSS, version 22

Results: The groups receiving 250 or 500 mg/kg RC had significantly lower immobility time [159.4 +/- 4.7 and 150.1 +/- 3.1 s] compared to the sham control group [192.1 +/- 7.8 s] in the forced swimming test, and a higher discrimination index [0.39 +/- 0.02 and 0.48 +/- 0.03] was seen in diabetic animals in the NOR task compared to the sham control group [0.2 +/- 0.01]

Also, the groups receiving treatment with RC [250 and 500 mg/kg] had significantly higher TAG [0.92 +/- 0.04 and 0.96 +/- 0.05 mmol/L] and lower MDA [0.76 +/- 0.02 and 0.67 +/- 0.03 nmol/mg protein] levels in the brains in comparison to the model group. In the 3rd and 4th weeks of study, the RC-treated mice [250 and 500 mg/kg] gained more weight [31.2 +/- 0.3 and 32.4 +/- 0.3 g, and 31.3 +/- 0.2 and 33.7 +/- 0.3 g, respectively] than the diabetic group [30 +/- 0.2 and 29.6 +/- 0.3 g]

Conc/us/on:This study showed that RG attenuated impairment of recognition memory and depressive-like behavior probably through modulation of oxidative stress in an STZ model of diabetes in mouse brains

Amyloid-beta: a crucial factor in Alzheimer's disease

Alzheimer's disease [AD] is the most prevalent form of dementia which affects people older than 60 years of age. In AD, the dysregulation of the amyloid-beta [Abeta] level leads to the appearance of senile plaques which contain Abeta depositions. Abeta is a complex biological molecule which interacts with many types of receptors and/or forms insoluble assemblies and, eventually, its nonphysiological depositions alternate with the normal neuronal conditions. In this situation, AD signs appear and the patients experience marked cognitional disabilities. In general, intellect, social skills, personality, and memory are influenced by this disease and, in the long run, it leads to a reduction in quality of life and life expectancy. Due to the pivotal role of Abeta in the pathobiology of AD, a great deal of effort has been made to reveal its exact role in neuronal dysfunctions and to finding efficacious therapeutic strategies against its adverse neuronal outcomes. Hence, the determination of its different molecular assemblies and the mechanisms underlying its pathological effects are of interest. In the present paper, some of the well-established structural forms of Abeta, its interactions with various receptors and possible molecular and cellular mechanisms underlying its neurotoxicity are discussed. In addition, several Abeta-based rodent models of AD are reviewed