Abstract
Focal cerebral ischemia-reperfusion injury is closely related to hyperglycemia and gut microbiota imbalance, while gut microbiota contributes to the regulation of brain function through the gut-brain axis. Previous studies in patients with diabetes have found that 'yam gruel' is a classic medicated diet made from Dioscorea polystachya, increases the content of Bifidobacterium, regulates oxidative stress, and reduces fasting blood glucose levels. The research reported here investigated the effects of 'yam gruel' on the cognitive function of streptozotocin-induced diabetic rats with focal cerebral ischemia-reperfusion injury and explored the mechanism underlying the role of the gut-brain axis in this process. 'Yam gruel' was shown to improve cognitive function as indicated by increased relative content of probiotic bacteria, and short-chain fatty acids in the intestinal tract and cerebral cortex reduced oxidative stress and inflammatory response and promotion of the expression of neurotransmitters and brain-derived neurotrophic factor. Thus, it is concluded that 'yam gruel' has a protective effect on cognitive function via a mechanism related to the gut-brain axis.
Highlights
Diabetes and stroke are common and frequently-occurring diseases that are closely related and often occur together
Gut microbiota and their metabolites, oxidative stress, inflammatory response, neurotransmitter, and BDNF and cognitive function-related indicators were significantly improved after the administration of 'yam gruel.' It is suggested that 'yam gruel' improves the cognitive function of diabetic rats with focal cerebral ischemia-reperfusion injury via the gut-brain axis
hematoxylin and eosin (HE) staining showed cell necrosis in the model group that was significantly improved by a 'yam gruel' diet
Summary
Diabetes and stroke are common and frequently-occurring diseases that are closely related and often occur together. Cerebral ischemia caused by a stroke can lead to reperfusion injury, which eventually aggravates brain tissue damage and dysfunction (Lin et al, 2016; Yang et al, 2019). Diabetes is a metabolic disease characterized by hyperglycemia that aggravates brain damage caused by acute stroke via a mechanism possibly related to hyperglycemia-induced oxidative stress and inflammatory response (Li et al, 2010). Studies have reported that long-term hyperglycemia generates a considerable number of oxygen free radicals in the brain. Excessive oxidation reaction increases vascular oxygen consumption and pressure, and the production of oxygen free radicals. Hyperglycaemia increases blood viscosity and leads to atherosclerosis and thrombosis, which further aggravates cerebral ischemia-reperfusion injury (Chehaib et al, 2016; Chorepsima et al, 2017)
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