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Cognitive deficit is an emerging health concern in diabetic patients. Hyperglycemia and reactive
oxygen species are believed to be among the prime candidates mediating the behavioral
impairments and memory deficits. The aim of this study was to evaluate the effect of curcumin on
blood glucose level, neurobehavioral responses and some oxidative stress biomarkers in Alloxan-
induced diabetic Swiss Albino mice. The animals were divided into five (5) groups of four mice
each (n=4). Diabetes was induced using a single dose of Alloxan (150 mg/kg) intra peritoneally.
Group Iserved as normoglycemic control and received distilled water, group II, III, IV and V were
diabetic and received olive oil 1 ml/kg, glibenclamide 1 mg/kg, curcumin 50 mg/kg and curcumin
100mg/kg respectively. All administrations were done for a duration of 21 days. Blood glucose
level was determined using glucose oxidase method and cognitive impairment was determined
using spontaneous alternation in the Y-maze and novel object recognition task (NORT). The result
obtained from this study showed that curcumin at both doses (50 mg/kg and 100 mg/kg) decrease
significantly (p < 0.05) the fasting blood glucose level (108.25 ± 16.01 mg/dl and 114.75 ± 5.56
mg/dl respectively) when compared with the diabetic control group (221.50 ± 14.03 mg/dl). Also
the result demonstrated that curcumin at 100 mg/kg significantly(p <0.05)increasethe percentage
alternation (74.39 ± 8.06%) when compared with the diabetic control group (47.50 ± 13.65%) in
the Y- maze test and significantly (p < 0.05) improve the memory, recognition and discrimination
indices (14.85 ± 6.46s, 0.39 ± 0.04s and 63.71 ± 2.95s) compared to the pretreatment (-10.90 ±
6.40s, -0.27 ± 0.11s and 36.04 ± 8.19s respectively) using NORT. Also, both doses of curcumin
recorded increase in SOD (12.84 ± 0.84) and catalase (85.05 ± 3.23) compared to the diabetic
control group (5.75 ± 0.96 and 62.27 ± 7.07) respectively. The findings of this study suggest that
curcumin has both antihyperglycemic and antioxidant activity and may ameliorate diabetes-
induced cognitive impairment in Swiss albino mice.
Diabetes mellitus has been considered as one of the major health concerns all around the world
today (Stoler et al., 2008). Experimental animal models are one of the best strategies for the
understanding of pathophysiology of any disease in order to design and develop the drugs for its
treatment (Chatzigeorgiou et al., 2009). Numerous animal models have been developed for the
past few decades for studying diabetes mellitus and testing anti-diabetic agents that include
chemical, surgical and genetic manipulations (Etuk, 2012). One of the most potent methods to
induce experimental diabetes mellitus is chemical induction by Alloxan (Tyberg et al., 2001). It is
a well- known diabetogenic agent that is used to induce Type I diabetes in experimental animals
(Viana et al., 2004).
Diabetes mellitus is recognized by chronic hyperglycaemia and is associated with long term
damage, dysfunction and failure of various body organs by involvement of micro and macro-
vasculature (Hink et al., 2005). The micro-vascular involvement mostly effects retina, renal
glomeruli and peripheral nerves, while macro-vascular involvement results in dyslipidemia,
formation of reactive oxygen species (ROS), advance glycation end product (AGEs), platelet
hyper-reactivity and endothelial dysfunction (Cosentino et al., 2003). Disturbance in endothelial
function and coagulation pathway may lead to platelet activation, adhesion and aggregation
(Ronald and Goldberg, 2012).
A large number of anti-diabetic medicines are available in the pharmaceutical market for diabetes
and its related complications; however, currently no effective therapy is available to cure the
disease (Sundaram and Mitra, 2007). WHO Expert Committee on Diabetes has recommended
investigatingtraditional herbal medicines, and in this regard morethan 400 medicinal plant species
have been compiled (WHO, 2010). These herbal products are gaining popularity in developing
and developed countries due to their lesser side effects and low cost (Sundaram and Mitra, 2007).
Cognitive function is defined as cerebral activities that lead to knowledge, including all means and
mechanisms of acquiring information. It encompass reasoning, memory, attention, and language
and lead directly to the attainment of information and thus, knowledge. Cognitive impairments in
the diabetic population are emerging problems that warrant immediate research attention.
Evidences from neurocognitive tests suggest that cognitive dysfunction should belisted along with
retinopathy, neuropathy, nephropathy and cardiovascular complications as one of the
complications of diabetes (Sima, 2010).
The major concerns regarding cognitive impairments in the diabetic population are the associated
dramatic rise in morbidi
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