Type-I diabetes aggravates post-hemorrhagic stroke cognitive impairment by augmenting oxidative stress and neuroinflammation in mice

被引:18
|
作者
Bahader, Ghaith A. [1 ]
Nash, Kevin M. [1 ]
Almarghalani, Daniyah A. [1 ]
Alhadidi, Qasim [1 ]
McInerney, Marcia F. [1 ]
Shah, Zahoor A. [1 ]
机构
[1] Univ Toledo, Dept Med & Biol Chem, Coll Pharm & Pharmaceut Sci, Toledo, OH 43614 USA
基金
美国国家卫生研究院;
关键词
Diabetes; ICH; Neuroinflammation; HMGB1; Cognitive impairment; EXPERIMENTAL INTRACEREBRAL HEMORRHAGE; NITRIC-OXIDE SYNTHASE; BRAIN-INJURY; ACUTE HYPERGLYCEMIA; TNF-ALPHA; T-MAZE; GLUTAMATE; STREPTOZOTOCIN; INFLAMMATION; EXPRESSION;
D O I
10.1016/j.neuint.2021.105151
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Diabetes Mellitus (DM) is a major comorbid condition that increases susceptibility to stroke. Intracerebral hemorrhage (ICH), a devastating type of stroke, accounts for only 13% of the total stroke cases but is associated with higher mortality. Multimorbid models of DM and ischemic stroke have been widely studied; however, fewer pieces of evidence are available on the impact of DM on the outcomes of ICH injury. In this study, we investigated the effect of DM on ICH-induced injury and cognitive impairments. Streptozotocin (STZ) induced type-I DM (T1DM) animal model was used, and experimental ICH was induced by intrastriatal injection of collagenase. Our results demonstrated that DM is associated with a significant increase in hematoma volume and deficits in post stroke locomotor, sensorimotor, and cognitive behavior in mice. The levels of neuroinflammation, oxidative/ nitrosative stress, and glial cell activation were also increased in the diabetic mice following ICH injury. This study provides a better understanding of the influence of DM comorbidity on hemorrhagic stroke outcomes and uncovers the important pathological mechanisms underlying DM-induced exacerbation of ICH injury.
引用
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页数:14
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