BackgroundKhaya grandifoliola (C.D.C.) stem bark, Cymbopogon citratus (Stapf) and Cryptolepis sanguinolenta (Lindl.) Schltr leaves are used in Cameroonian traditional medicine for the treatment of inflammatory diseases. Several studies have been performed on the biological activities of secondary metabolites extracted from these plants. However, to the best of our knowledge, the anti-neuro inflammatory and protective roles of the polysaccharides of these three plants have not yet been elucidated. This study aimed at investigating potential use of K. grandifoliola, C. sanguinolenta and C. citratus polysaccharides in the prevention of chronic inflammation.MethodsFirstly, the composition of polysaccharide fractions isolated from K. grandifoliola stem bark (KGF), C. sanguinolenta (CSF) and C. citratus (CCF) leaves was assessed. Secondly, the cytotoxicity was evaluated on Raw 264.7 macrophages and U87-MG glioblastoma cell lines by the MTT assay. This was followed by the in vitro evaluation of the ability of KGF, CSF and CCF to inhibit lipopolysaccharides (LPS) induced overproduction of various pro-inflammatory mediators (NO, ROS and IL1β, TNFα, IL6, NF-kB cytokines). This was done in Raw 264.7 and U87-MG cells. Finally, the in vitro protective effect of KGF, CSF and CCF against LPS-induced toxicity in the U87-MG cells was evaluated.ResultsCCF was shown to mostly contain sugar and no polyphenol while KGP and CSP contained very few amounts of these metabolites (≤ 2%). The three polysaccharide fractions were non-toxic up to 100 μg.mL− 1. All the polysaccharides at 10 μg/mL inhibited NO production, but only KGF and CCF at 12.5 μg/mL down-regulated LPS-induced ROS overproduction. Finally, 100 μg/mL LPS reduced 50% of U87 cell viability, and pre-treatment with the three polysaccharides significantly increased the proliferation.ConclusionThese results suggest that the polysaccharides of K. grandifoliola, C. citratus and C. sanguinolenta could be beneficial in preventing/treating neurodegenerative diseases in which neuroinflammation is part of the pathophysiology.
Neuropathic pain is caused by structural lesion leading to functional abnormalities in central and peripheral nervous system. Neuropathic pain in itself is not always a disease, as it arises due to consequences of other diseases like diabetes, spinal cord injury, degenerative neuronal diseases and cancer. Current strategies of neuropathic pain treatment have provided relief to the patients to some extent, but complete cure is still a distant dream. In the future, it is hoped that a combination of new and improved pharmaceutical developments combined with careful clinical trials and increased understanding of neuroplasticity will lead to improved and effective pain management strategies leading to improved quality of life. In this review we have discussed various therapeutic targets of neuropathic pain and their pathophysiological mechanisms. Current status of drugs used for treatment of neuropathic pain have also been discussed in the review.
Aims: To determine the effects of polysaccharide fractions named KGF and CCF respectively for Khaya grandifoliola stem bark and Cymbopogon citratus leaves on Central Nervous System (CNS) depression and on systemic lipopolysaccharide (LPS)-induced brain inflammation and hyperalgesia in BALB/c.
Methodology: BALB/c mice weighing about 25-35 g were used for the experimentation. Depressant effects of polysaccharide fractions were firstly evaluated using Rota Rod and Actophotometer apparatus. Secondly, LPS or saline solution (5 mg/kg) was Intraperitoneally administered (i.p.) 1 hour after oral administration of polysaccharide fractions (100 mg/kg test dose, p.o.) or distilledwater. Then, the hot plate and tail-flick models were performed 1 hour after LPS injection to determine thermal hyperalgesia and brain inflammation, was examined 3 hours after LPS injection by Luminex assay.
Results:Systemic LPS administration resulted in a reduction of pain response latency and an increasing expression of nuclear factor-κB (NF-κB) and pro-inflammatory cytokines interleukin-1β (IL-1β), IL-6, tumor necrosis factor- α (TNF-α) genes in brain after 24 hours. From the results it was observed that treatment with KGF and CCF (100 mg/kg, p.o) significantly attenuated LPS-induced hyperalgesia and overexpression of brain levels of IL-1β, IL-6 and TNF-α genes dependent on inhibition of the NF-κB signaling pathway in BALB/c without CNS depressant properties.
Conclusion: The present findings confirm the potential of KGF and CCF in the treatment of neuroinflammation-related diseases and it warrant further testing for the development of a new chemical entities. However further studies are required for determination of effective dose and mechanism of action associated.
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