Nigerian scientists have developed an animal model which demonstrates that Jobelyn ® Supplement lowered Neuronal Degeneration. The team of scientists led by Oyinbo A. Charles Department of Human Anatomy, Faculty of Basic Medical Sciences College of Health Sciences, Niger Delta University Wilberforce Island, Bayelsa State (Nigeria) in an interview said that Alcohol-induced neurodegeneration, a consequence of chronic ethanol exposure, is a neuroadaptation that drives the progression of alcohol use disorder (AUD). Unfortunately, conventional drugs for AUDs do not prevent neurodegeneration as part of their pharmacological repertoire. Multimodal neuroprotective therapeutic agents are hypothesized to have high therapeutic utility in the treatment of central nervous system. Interestingly, nutraceuticals by nature are multimodal in mechanisms of action. Purpose: This study examined the neuroprotective potential of Jobelyn in prefrontal cortex (PFC) of a binge-alcohol rat model of AUD. The result of the animal experiment showed that Jobelyn supplementation significantly lowered the levels of histologic and biochemical indices of neurodegeneration, and caused an increased expression of p53 protein and a decreased expression of NSE immunoreactivity (NSE-IR). The scientists concluded that Jobelyn supplementation ameliorates neurodegeneration in the PFC of AUD rats by reducing the oxidative stress, reducing the NSE-IR, and by increasing the expression of cellular tumor antigen p53 in the cortical neurons
Explaining why this study was very important Dr. Oyinbo said that Excessive alcohol ingestion, characteristic of alcohol use disorders (AUDs), results in neurodegeneration, which is responsible for the cognitive and behavioral impairment that drives the transition to alcohol addiction . Globally, about 80 million people have diagnos-able AUDs, making it a major global health concern. To date, renowned medications for the treatment of AUDs: acamprosate, disulfiram, and naltrexone, have been clinically unsatisfactory. They targeted the psychoactive properties of alcohol; while the neurodegenerative effect of alcohol that drives alcohol-induced neurological dysfunction was not managed by these specific remedies. The prefrontal cortex (PFC) is highly susceptible to alcohol-induced damage . PFC deficiency is characterized by executive dysfunction such as deficits in working memory, impulse control, and decision making. They are linked with the inability to abstain from alcohol. Executive dysfunction often occurs before general mental status challenges. Studies showed that chronic alcohol exposure is related to the induction of oxidative stress and neuroinflammatory mediators, which lead to neurodegeneration. Consistent with this hypothesis, antioxidants have been effective in reducing binge alcohol-induced neurodegeneration. Neuroprotection mediated by antioxidant treatment is associated with the inhibition of nuclear factor kappalight-chain-enhancer of activated B cells–DNA binding, reduction of cyclooxygenase-2 (COX-2) expressions, and microglial activation; which support the hypothesis that neuroinflammatory signalling and oxidative stress contribute to alcohol-induced neurodegeneration. Jobelyn (Health Forever Products, Lagos, Nigeria), a commercially available nutraceutical, has shown outstanding anti-inflammatory and anti-oxidative properties. Interestingly, it is on record that Jobelyn’s oxygen radical absorbance capacity value (37,622 μmol/TE/g) is the highest thus far recorded in any known plant. Jobelyn’s strong anti-oxidative and anti-inflammatory properties have been utilized in the management and treatment of myriad diseases ranging from cancer, sickle cell, diabetes, arthritis, infertility, and many other diseases. Jobelyn demonstrated a selective COX-2 inhibition property, thus providing an effective reduction in inflammation without side effects of common prescription medications. Although, multimodal neuroprotective agents are considered to have a high therapeutic utility in the treatment of neurodegenerative diseases, there is yet the dilemma of how to safely combine individuals’ conventional agents into a single agent with multimodal mechanisms of neuroprotection. Nutraceuticals by nature are multimodal in mechanism; they produce a vast array of diverse chemical substances in a natural form in an entity, and any search of these resources for unusual or enhanced biological properties can expect some degree of success. Hence, this study was aimed at assessing the neuroprotective potentials of Jobelyn in the PFC of rats with AUD.
In conclusion, the scientists said that the study has demonstrated the potentials of Jobelyn (a nutraceutical) in the quest for a remedy for AUDs. Till date, acamprosate, disulfiram, and naltrexone, which are the approved pharmacotherapeutic interventions for the treatment of AUDs have left much to be desired. Jobelyn’s strategy of preventing neurodegeneration from within the neurons safeguards them ad initium. Coupled with this, it also safeguards the neuropil by neutralising the assault of free radical. Therefore, the neuroprotective mechanisms of Jobelyn in alcohol-induced cortical neurodegeneration involve an increase in p53 protein expression, a decrease in ɤ-enolase proteins expression, and an alleviation of oxidative stress.
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