Article ID Journal Published Year Pages File Type
6265144 Brain Research 2011 9 Pages PDF
Abstract

An understanding of the diabetes-related changes in brain proteome composition in diabetes and treatment with Cynodon dactylon may provide insights to understand the brain function associated diabetes and metabolic protein mechanism responsible for this disease and in order to discover novel preventive and therapeutic drugs. We have performed a comprehensive proteomic analysis for comparison of rat brain proteome by using advance 2-dimensional electrophoresis (2DE) combined with mass spectrometry (MALDI-TOF-MS). We report here a comparison of alloxan-induced type 1 diabetic rats and C. dactylon-treated diabetic rats at 2 weeks following diabetes onset. As a result, we identified two differentially expressed proteins from rat brain. The identified proteins were functionally classified into two groups: (i) metabolic signalling protein (PPP1R14D) and ii) vesicle transport signalling protein (RAB18). This study provides a preliminary reference map of normal rat brain that will form a basis for comparative studies on normal and pathological conditions of the brain connected with diabetes and may serve as a potential tool for clinical diagnosis, therapeutics and prognosis and may provide new insights into novel mechanisms and therapeutic targets for diabetes-associated neurological disorder.

Research Highlights► Dysfunctional insulin has an impact on major diseases such as neurodegenerative disorder. ► PPP1R14D and RAB18 are predominantly expressed in diabetic condition. ► PPP1R14D is mainly involved in glycogen breakdown and glycogen synthesis. ► RAB18 is mainly involved in dramatic redistribution vesicular transport in cell. ► Over-expression of PPP1R14D inhibits the function of PP1; hence, switch-on glycogen breakdown and switch-off glycogen synthesis. ► Over-expression of RAB18 leads to uneven distribution of protein inside the cell causes neurological disorder. ► C. dactylon extract were down-regulated the expression of PPP1R14D and RAB18 in treated rats.

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