Polysaccharides, Next Potential Agent for the Treatment of Epilepsy?

Abstract

Epilepsy is a chronic neurological disorder. Current pharmacological therapies for epilepsy have limited efficacy that result in refractory epilepsy (RE). Owing to the limitations of conventional therapies, it is needed to develop new anti-epileptic drugs. The beneficial effects of polysaccharides from Chinese medicines, such as Lycium barbarum polysaccharides (COP) and Ganoderma lucidum polysaccharides (GLP), for treatment of epilepsy include regulation of inflammatory factors, neurotransmitters, ion channels, and antioxidant reactions. Especially, polysaccharides could be digested by intestinal microbial flora, referred as “intestinal brain organ” or “adult’s second brain”, may be the target for treatment of epilepsy. Actually, polysaccharides can effectively improve the type and quantity of intestinal flora such as bifidobacteria and lactic acid bacteria and achieve the purpose of treating epilepsy. Therefore, polysaccharides are hypothesized and discussed as potential agent for treatment of epilepsy.

Neuroprotective, neurogenic, and anticholinergic evidence of Ganoderma lucidum cognitive effects: Crucial knowledge is still lacking

“…Such pathophysiological pathway could be an interesting target to G. lucidum compounds, especially polysaccharides. Besides, although these compounds are not capable of crossing the blood–brain barrier, the polysaccharides can modulate peripheral inflammation, oxidative stress, or even intestinal dysbiosis 66 . We highlight the need for studies involving the modulating effect of G. lucidum components on dysbiosis, as this mushroom is accepted as a nutraceutical element and the evidence of the polysaccharides in the regulatory function of the intestinal microbiota 66 …”

“…Regarding inflammatory pathways, an increase in the Gram‐negative bacteria population seems to result in mild chronic inflammation, affecting the homeostasis of the intestinal epithelium, which increases the permeability to the leakage of bacterial toxins into the systemic circulation, contributing to mechanisms of neuroinflammation, oxidative stress, neuronal apoptosis, which constitute the pathophysiology of cognitive disorders, such as AD 67 . In vitro studies reported that G. lucidum oligosaccharides increase the amount of beneficial (i.e., Lactobacillus , Bifidobacterium , Faecalibacterium , and Prevotella ) and decrease the relative abundance of noxious bacteria (i.e., Escherichia , Shigella , and Dorea ), contributing to health gut and preventing dysbiosis 66,68 . In addition, studies demonstrated that polysaccharides with different molecular weights inhibit the secretion of proinflammatory cytokines (i.e., TNF‐α, IL‐1β, and IL‐6) in the inflammation model induced by lipopolysaccharides in human colorectal adenocarcinoma cells (pretreatment for 2 h at final concentrations of 10, 50, and 200 µg/mL) and in mice dextran sulfate sodium‐induced colitis (pretreatment at doses 10, 50, and 200 mg, for 7 days), recovering inflamed mice colonic tissues 69 …”

“…Besides, although these compounds are not capable of crossing the blood-brain barrier, the polysaccharides can modulate peripheral inflammation, oxidative stress, or even intestinal dysbiosis. 66 We highlight the need for studies involving the modulating effect of G. lucidum components on dysbiosis, as this mushroom is accepted as a nutraceutical element and the evidence of the polysaccharides in the regulatory function of the intestinal microbiota. 66 It has been proposed that gut dysbiosis can induce cognitive dysfunction through neural, inflammatory, and biochemical mechanisms.…”

“…66 We highlight the need for studies involving the modulating effect of G. lucidum components on dysbiosis, as this mushroom is accepted as a nutraceutical element and the evidence of the polysaccharides in the regulatory function of the intestinal microbiota. 66 It has been proposed that gut dysbiosis can induce cognitive dysfunction through neural, inflammatory, and biochemical mechanisms. 67 Regarding inflammatory pathways, an increase in the Gram-negative bacteria population seems to result in mild chronic inflammation, affecting the homeostasis of the intestinal epithelium, which increases the permeability to the leakage of bacterial toxins into the systemic circulation, contributing to mechanisms of neuroinflammation, oxidative stress, neuronal apoptosis, which constitute the pathophysiology of cognitive disorders, such as AD.…”

“…However, if these events can contribute to preventing cognitive impairments is still unclear and needs further investigation. Nonetheless, it has been proposed that by modulating the intestinal microbiota health, polysaccharides can elicit benefits in disorders, such as epilepsy, or even trigger the sleep process, which suggests that the regulation of gut microbiota can exert beneficial effects on CNS 66,70 …”