Neuroprotective Effect of Quercetin on the Duodenum Enteric Nervous System of Streptozotocin-Induced Diabetic Rats

Abstract

Supplementation with quercetin eased the damage caused by diabetes, promoting a neuroprotective effect and reducing enteric glial loss in the duodenum.

Combination vitamin C and vitamin E prevents enteric diabetic neuropathy in the small intestine in rats

“…In addition to the reduction of neuronal density, hypertrophy of the cell body area occurred of NADH-d + neurons in the duodenum (37.8%) and in the ileum (35.8%), possibly in an attempt to maintain physiological conditions of the neurons that survived. Similar results were reported in previous studies in diabetic rats (Pereira et al 2011;Lopes et al 2012;Hermes-Uliana et al 2014). Adaptive mechanisms of the remaining neurons attempt to compensate for neuronal loss by increasing protein synthesis to maintain their function and target tissue (Zanoni et al 2002;Hermes-Uliana et al 2014).…”

“…Thus, we can infer that diabetes promoted a reduction of neuron metabolism, leading to the death of a portion of its neuronal population. We observed a reduction of more than half of these neurons, and diabetic neuropathy was observed, similar to studies that used other experimental models of diabetes and evaluated different regions of the gastrointestinal tract, including the stomach (Takahashi et al 1997;Fregonesi et al 2001), duodenum (Pereira et al 2006;Zanoni et al 2011;Lopes et al 2012), jejunum (Defani et al 2003;De Freitas et al 2008;Alves et al 2010;HermesUliana et al 2014), ileum Shotton and Lincoln 2006;Pereira et al 2011), cecum (Zanoni et al 1997;Zanoni et al 2011), and proximal colon (Tashima et al 2007;Roldi et al 2009). The development of neuropathy affects different types of enteric neurons, which are responsible for the control of important functions, such as motility, secretion, blood flow, and growth aspects of the local mucosal immune system (Furness 2012).…”

“…Among the chronic complications caused by diabetes, neurological manifestations are the most common, affecting both the autonomic and peripheral nervous systems and impairing the quality of life of patients (Chandrasekharan et al 2011). Our research group found that diabetes mellitus reduced the density of myenteric neurons and enteric neural plasticity in various segments of the digestive system (Takahashi et al 1997;Zanoni et al 1997;Fregonesi et al 2001;Defani et al 2003;Zanoni et al 2003;Pereira et al 2006;Tashima et al 2007;Zanoni et al 2007;De Freitas et al 2008;Roldi et al 2009;Alves et al 2010;Pereira et al 2011;Zanoni et al 2011;Lopes et al 2012;Hermes-Uliana et al 2014). These changes in enteric innervation that arise from diabetes are attributable to persistent hyperglycemia that produces numerous metabolic changes.…”

Recent trends in the development of nanophytobioactive compounds and delivery systems for their possible role in reducing oxidative stress in Parkinson’s disease models

“…This bioflavonoid has multiple neurobeneficial activities, such as free radical scavenging, antianxiety, neuroprotection, and cognitive enhancing effects. [191][192][193] Quercetin is chemo labile and thermo labile, which leads to lower bioavailability at the target site. 194 In addition, quercetin has poor solubility and distribution, resulting in less bioavailability to the brain.…”

Morphoquantitative Study of Rattus norvegicus Submucosal Plexus by Different Neuronal Evidentiation Histochemical Techniques

“…In adult mice, Young & Ciampoli (1998) estimated that the nitrergic neuron population was 3 %. However, studies on jejunum (Hermes-Uliana et al, 2014) and duodenum (Lopes et al, 2012) of 210-day-old rats found 26 % and 23 % of nitrergic neurons in the submucosal plexus, respectively. A greater density of NADPH-d + neurons and a greater expression of NOS in aging process rats was verified by several authors that have related this finding to a greater resistance of these neurons to nutritional deficiencies (Sant'Ana et al, 2012a), degenerative processes caused by aging and by chronic degenerative diseases (Fregonesi et al, 2004), and NOS expression by neurons that did not use to express it but start doing it when initiating the cell death process (Fregonesi et al).…”