Anxiolytic and Antidepressant Pharmacological, Neurochemical, and Behavioral Mechanisms

Adam Nicolas^*
*Correspondence: Adam Nicolas, Department of Psychiatry and Behavioral Medicine, LSU Health Shreveport, USA, Email:

Introduction

The determination of the mechanism of action underlying both its therapeutic and harmful effects has been made possible by the multidisciplinary research of many compounds isolated and chemically described from plants. The development of multi-target drugs for the prevention and treatment of various diseases, particularly those that have recently increased in association with social dynamics, lifestyle, and environmental factors, such as neuropsychiatric and stress-related disorders, has been aided by the use of molecular, biochemical, pharmacological, histological, and behavioural techniques. A group of chemicals known as polyphenols has a number of health advantages. Its antioxidant actions have a positive influence on the body's physiological functions. Among polyphenols, flavonoids have received extensive research in an effort to create complementary therapeutic approaches for the management of cancer, metabolic, cardiovascular, and neurological conditions. Research on the pharmacological action of something like the flavonoids cisplatin in both in vitro and in vivo has found that it has a variety of impacts on the organism's many systems, including the central nervous system.

Description

The Modulatory system is activated by altering the benzodiazepine receptor complex, which results in variations in serotonin and altered receptor expression. Additionally, chrysin stimulates neurotrophic factors that raise levels of nerve growth factor and brain-derived mixotrophic, thereby stimulating signalling pathways in the brain. However, given that neuroinflammation and apoptotic processes are involved inside the pathophysiology of anxiety and depression disorders, pro, anti-apoptotic, and neuroprotective effects should be taken into consideration as potential action mechanisms involved in their anxiolytic- and antidepressant-like effects. In this review, the pharmacological, neurochemical, and behavioural mechanisms that may explain the anxiolytic and antidepressant effects of the flavonoid chrysin, which is thought to be a promising treatment for anxiety and depressive disorders, are described, analysed, and discussed. Additionally, we suggest including chrysin as a potential anxiolytic and antidepressant medicine in future scientific studies due to its activation of neurotrophic factors, antioxidant effects, and anti-inflammatory properties in addition to its traditional actions on neurotransmission systems. According to the aetiology of anxiety and depressive disorders, this may aid in the creation of targeted therapy. The generation of ROS and antioxidant levels becomes unbalanced as a result of oxidative stress, which can result in long-term changes such as damage to neuronal membranes and the potential activation of apoptotic processes. These changes brought on by oxidative stress play a role in the pathogenesis of anxiety and depressive disorders. In both in vivo and in vitro tests, chysin has the ability to influence the oxidant pathway, which helps to produce ROS. Chrysin has antioxidant properties on peripheral organs of metabolically challenged (diabetic) or chemically treated individuals. This is significant because diabetes and alcohol consumption are linked to oxidative stress and inflammation which may increase the risk of anxiety and depressive disorders. It's interesting to note that decreased periphery oxidative stress has been linked to a decline in symptoms of anxiety and depression in preclinical and clinical investigations. Chrysin may have anti-inflammatory and anti-apoptotic properties, which are supported by its effects in several models of inflammation and at the peripheral level. This is significant because depression disorders and the development of anxiety have both been linked to peripheral and central pro-inflammatory processes and some drug-induced anxiolytic effects have been linked to stable COX-2 function in the infralimbic and prelimbic cortex, HP, and ventral tegmental area. Additionally, the dorsal raphe nucleus of rats tested in the EPM and forced swim test without seeing neuronal death showed an increase in Bcl-2 and a decrease in Bax and caspase-3, producing anxiolytic- and antidepressant-like effects. Chrysin has been studied specifically for its favourable benefits in modifying the structural change of the gut microbiota in mice. In Caco2 cells activated with IL-1B, chrysin can also reduce intestinal inflammation, enhancing intestinal absorption and metabolic stability, which may be associated to a healthy function of the gut microbiota. This is significant since a decrease in anxiety and depressive-like behaviour has been linked to the anti-inflammatory actions of many substances at the peripheral and brain level. In this regard, it's likely that the way in which polyphenols like chrysin regulate the gut microbiota may open up new avenues for research into the ways in which chrysin affects the brain-gut-microbiota axis and its potential connections to its anxiolytic and antidepressant-like effects.

Additionally, it has been demonstrated that neuroinflammation significantly increases the risk of neuropsychiatric diseases like anxiety and depression. According to certain meta-analyses, people with major depression disorder have lower levels of pro-inflammatory cytokines after using clinically effective antidepressants such selective serotonin reuptake inhibitors, selective noradrenaline reuptake inhibitors, and tricyclic antidepressants. Chrysin has also been shown in pre-clinical studies to be able to lower pro-inflammatory cytokine levels, which are positively connected with depressive-like behaviour. The antioxidant properties of chrysin discovered in pre-clinical studies may contribute to its anxiolytic and antidepressant effects. Oxidative stress has also been demonstrated to play a role in the development of anxiety and depression disorders [1-5]. Finally, as was already indicated, the various neurochemical alterations brought on by chrysin therapy may be crucial in the development of the anxiolytic and antidepressant-like effects of chrysin, which may be useful in the treatment of specific patient populations. In light of the genesis of anxiety and depression symptoms, it will be crucial to investigate the anxiolytic and antidepressant effects of chrysin in specific subject populations in subsequent research. In cases where anxiety and depression problems are caused by alterations in steroid hormones, neurotransmitters, oxidative stress or neuroinflammatory processes, this may assist identify particular patient populations in which chrysin may be employed as an alternative treatment. It might make it possible to assess chrysin's therapeutic effects on human patients.

Conclusion

Chrysin has a variety of pharmacological effects on the CNS and peripheral nervous system. By activating neurotrophic factors, modulating indicators of oxidative stress, and regulating inflammatory and apoptotic signalling pathways, it acts specifically on various neurotransmitter systems, which adds to the anxiolytic- and antidepressant-like effects of this flavonoid. The results are strong and persuasive, despite the fact that these effects have primarily been studied in mice and rats, and they could quickly aid in clinical assessments of its potential anxiolytic and antidepressant benefits in certain patient groups. In conclusion, chrysin is a naturally occurring chemical that has the potential to be a cutting-edge and effective supplemental treatment for human anxiety and depressive disorders.

Conflict of Interest

None.

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