MO11 and MS06 ameliorated cadmium chloride-induced neuro-inflammation, hyperplasia and apoptosis via NF-kB/Caspase-3/p53 pathway and down-regulated sVEGFR in rats

Abstract

Cadmium is a neurotoxin, carcinogen and a suspected agent in aetiology of Parkinson’s disease and Alzheimer’s disease (AD). Furthermore, upregulations of Caspase3 and p53 were reported in brains of AD patients. This study evaluated the neuroprotective potentials of MO11 (isolated from Moringa oleifera leaves) and MS06 (isolated from Musa sapientum suckers) in Cadmium Chloride (CdCl)induced neurotoxicity in the cerebrum of rats. Twentyeight adult male wistar rats (average weight of 155 g) were randomly divided into 7 groups (n = 4). Group 1 received physiological saline. Groups 24 and 7 received single 1.5 mg/Kg bodyweight of CdCl (i.p.) (Day 1). Groups 34 and 7 were posttreated with 15 mg/Kg bodyweight of MO11, 15 mg/Kg bodyweight of MO11 + 7 mg/Kg bodyweight of MSF1 and 3.35 mg/Kg bodyweight of Doxorubicin respectively (Days 117). Groups 56 received only MO11 and Vegetable Oil (vehicle) respectively (Days 117). Cerebral histopathology (Cresyl Fast Violet method) was evaluated in rats. ELISA evaluations of biomarkers of pro-inflammation (IL1β, IL6, IL8 and NFkB), anti-inflammation (IL-4 and IL-10), apoptosis (Caspase3 and p53), proliferation (Ki67) and angiogenesis (sVEGFR) in cerebral homogenates of rats were also conducted. Histopathological evaluations showed a high number of chromatolytic cells in Group 2, compared with Groups 1 and 37. Posttreatments of CdClinduced neurotoxicity with MO11 and MS06 resulted in decreased levels of IL1β, IL6, IL8, NFkB, Caspase3, Ki67, p53 and sVEGFR, but increased levels of IL4 and IL10 in Groups 34, compared with Group 2. Therefore, MO11 and MS06 possess neuroprotective, neuroregenerative, anti-AD, anti-inflammatory and anticancer potentials.