Sinapic Acid Alleviates Oxidative Stress and Neuro-Inflammatory Changes in Sporadic Model of Alzheimer's Disease in Rats.

Vandna Verma,Reeta Kh,Devendra Singh

doi:10.3390/brainsci10120923

Abstract

The role of oxidative stress, neuro-inflammation and cholinergic dysfunction is already established in the development of Alzheimer’s disease (AD). Sinapic acid (SA), a hydroxylcinnamic acid derivative, has shown neuro-protective effects. The current study evaluates the neuro-protective potential of SA in intracerebroventricular streptozotocin (ICV-STZ) induced cognitive impairment in rats. Male Wistar rats were bilaterally injected with ICV-STZ. SA was administered intragastrically once daily for three weeks. Rats were divided into sham, ICV-STZ, STZ + SA (10 mg/kg), STZ + SA (20 mg/kg) and SA per se (20 mg/kg). Behavioral tests were assessed on day 0 and 21 days after STZ. Later, rats were sacrificed for biochemical parameters, pro-inflammatory cytokines, choline acetyltransferase (ChAT) expression and neuronal loss in the CA1 region of the hippocampus. The results showed that SA 20 mg/kg significantly (p < 0.05) improved cognitive impairment as assessed by Morris water maze and passive avoidance tests. SA 20 mg/kg reinstated the altered levels of GSH, MDA, TNF-α and IL-1β in the cortex and hippocampus. STZ-induced decreased expression of ChAT and neuronal loss were also significantly (p < 0.05) improved with SA. Our results showed that SA exhibits neuro-protection against ICV-STZ induced oxidative stress, neuro-inflammation, cholinergic dysfunction and neuronal loss, suggesting its potential in improving learning and memory in patients of AD.

Highlights

80% of cases of dementia are linked to Alzheimer’s disease (AD), making it the major form of dementia [1]
Our results showed that Sinapic acid (SA) exhibits neuro-protection against intracerebroventricular streptozotocin (ICV-STZ) induced oxidative stress, neuro-inflammation, cholinergic dysfunction and neuronal loss, suggesting its potential in improving learning and memory in patients of AD
AD like behavioral changes including decreased time spent in the fourth quadrant, enhanced escape latency in the Morris water maze test, decreased retention latency in the passive avoidance test, latency in the Morris water maze test, decreased retention latency in the passive avoidance test, impaired oxidative status accompanied by increased pro-inflammatory cytokines and decreased choline acetyltransferase (ChAT)

Summary

Introduction

80% of cases of dementia are linked to Alzheimer’s disease (AD), making it the major form of dementia [1]. The majority of the patients with AD have late onset called sporadic AD (>60 year), and less than 1% of patients have inherited mutations in genes that affect the processing of amyloid beta (Aβ) and these patients develop the disease at an early age (

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