Taiy Chemical
Neuromedin U-23 (rat)
Synonym Neuromedin U-23 (rat)
Species Rat
Protein Accession P0C818
Purity Greater than 95% by HPLC analysis
Endotoxin Level < 1 EU per 1 μg of protein
Biological Activity Not determined
Expression System Escherichia coli
Fusion Tag None
Predicted Molecular Mass 2767 Da
Formulation Lyophilized in 20mM Tris, 150mM NaCl, pH 7.5
Reconstitution Centrifuge vial before opening. Reconstitute in sterile ddH2O to a concentration of 0.1-1.0 mg/ml.
Storage & Stability Store at -20°C. For long term storage, it is recommended to store at -80°C. Avoid repeated freeze-thaw cycles.
FAQ
What is Neuromedin U-23 (rat) and why is it significant in scientific research?

Neuromedin U-23 (rat) is a potent neuropeptide that consists of 23 amino acids, primarily found in the gut but also expressed in the central nervous system. Its significance in scientific research stems from its diverse role in physiological processes. This neuropeptide has been linked to a wide range of functions in mammalian systems, including the regulation of smooth muscle contraction, blood pressure, and feeding behavior. Moreover, Neuromedin U has been shown to play a critical role in the stress response, energy homeostasis, and pain perception.

The study of Neuromedin U-23 provides insights into the complex interactions between the nervous and endocrine systems, making it a focal point for research on neuroendocrine signaling pathways. Researchers use Neuromedin U-23 in experimental studies to unlock the mechanistic pathways through which it exerts its effects. Identifying these pathways guides the development of therapeutic strategies for conditions like obesity, hypertension, and chronic pain, where Neuromedin U signaling may be dysregulated.

Neuromedin U-23 also garners interest due to its involvement in inflammatory processes. It influences immune activity, pointing to its potential role in modulating immune responses. Understanding its functions could lead to novel approaches in managing autoimmune disorders or inflammatory diseases. The use of Neuromedin U-23 in animal models, like rats, allows researchers to explore its physiological roles in a controlled environment, offering opportunities to decipher its functions that are conserved across species, including humans.

In addition, Neuromedin U-23 is a candidate for biomarker discovery. Its levels can reflect physiological and pathological states, potentially serving as an indicator of disease progression or response to therapy. By understanding its precise role in cellular communication and systemic regulation, researchers hope to employ Neuromedin U-23 in diagnostic and therapeutic applications, emphasizing its significance in both physiological and pathological contexts.

How does Neuromedin U-23 affect feeding behavior and energy homeostasis in rats?

Neuromedin U-23 (rat) plays a substantial role in regulating feeding behavior and energy homeostasis, primarily through its actions in the central nervous system. This neuropeptide has been identified in regions of the brain associated with the control of appetite and energy expenditure, including the hypothalamus, which is a critical hub for feeding regulation. Neuromedin U-23 is known to exert anorexigenic effects, meaning it reduces food intake, which is a focal point for researchers studying obesity and metabolic disorders.

Upon its release, Neuromedin U-23 interacts with specific receptors in the brain, such as Neuromedin U receptor 2 (NMUR2), to influence neuronal activities that regulate hunger signals. Studies have shown that intracerebroventricular administration of Neuromedin U-23 in rats leads to a decrease in food consumption. This action is believed to be mediated through the modulation of neuropeptide systems, including those involving leptin and insulin, which are pivotal in maintaining energy balance.

Furthermore, Neuromedin U-23 impacts energy homeostasis by influencing energy expenditure and metabolic rates. Its effect on thermogenesis, particularly in brown adipose tissue, suggests a mechanism through which it can increase energy expenditure, supporting its role in maintaining body weight. This property makes Neuromedin U-23 a molecule of interest for developing anti-obesity therapies that target energy balance rather than just appetite suppression.

In addition to nutritional influence, Neuromedin U-23 is implicated in the body's response to energy deficits and surpluses, helping to maintain metabolic equilibrium. By studying Neuromedin U-23's effects on appetite and energy expenditure in rat models, researchers can better understand its potential application in managing human metabolic diseases. The implications of Neuromedin U-23 on feeding behavior and energy regulation highlight its utility as both a research tool and a prospective target for therapeutic intervention in metabolic health.

What are the known physiological effects of Neuromedin U-23 on the cardiovascular system?

Neuromedin U-23 (rat) has been shown to exert significant physiological effects on the cardiovascular system. This neuropeptide influences cardiovascular functions by interacting with specific receptors expressed in cardiac and vascular tissues. Studies demonstrate that Neuromedin U-23 can modulate the contraction of smooth muscles in the blood vessels, which has direct implications for blood pressure regulation and cardiac function.

Neuromedin U-23 has a pronounced vasoconstrictive effect, particularly on blood vessels like the rat aorta. It induces vascular smooth muscle contraction, leading to increased vascular resistance, which, in turn, elevates blood pressure. This vasoconstrictive action is part of the body's complex mechanism to regulate blood flow and pressure, especially under conditions that require rapid cardiovascular adjustments.

Furthermore, Neuromedin U-23 is involved in cardiac stress responses. It may contribute to changes in heart rate and myocardial contractility, influencing the heart's capacity to pump blood efficiently. Its effect on cardiovascular function is of interest particularly in studying hypertension and other cardiovascular diseases where vascular tone regulation is disturbed.

On a systemic level, Neuromedin U-23 impacts the sympathetic nervous system, which is integral in cardiovascular regulation. It is thought to enhance sympathetic nervous activity, potentially influencing heart rate and vascular tone. This connection illustrates Neuromedin U-23’s role in integrating neuroendocrine signals with cardiovascular responses, supporting its involvement in stress-related cardiovascular adaptations.

Research on rats allows scientists to explore these cardiovascular effects in vivo, offering insights that can be extended to human physiology. The potential therapeutic targeting of Neuromedin U signaling pathways could lead to novel treatments for cardiovascular diseases, emphasizing the importance of understanding its precise role in the cardiovascular system. By further elucidating these effects, researchers aim to develop interventions that can mitigate cardiovascular dysfunction associated with disorders of vascular tone and blood pressure regulation.

How does Neuromedin U-23 influence pain perception in rats?

Neuromedin U-23 plays a notable role in modulating pain perception, with evidence suggesting it acts as a modulator of nociceptive pathways in the central nervous system. This neuropeptide interacts with receptors expressed in brain regions associated with pain processing, contributing to our understanding of the neurochemical basis of pain perception.

Research indicates that Neuromedin U-23 can influence both acute and chronic pain pathways. Its effects are mediated through interactions with specific receptors like NMUR2, which are prevalent in pain-associated circuitry. In experimental models, Neuromedin U-23 has been shown to exert pro-nociceptive effects, meaning it can enhance the sensation of pain. This action highlights its potential role in signaling pathways that amplify pain, suggesting Neuromedin U-23 might be involved in pain augmentation rather than relief.

Neuromedin U-23's involvement in pain modulation is also linked to its interaction with neuropeptides and neurotransmitters, such as substance P and calcitonin gene-related peptide (CGRP), which are crucial mediators of pain and inflammation. Its influence on these chemical messengers illustrates a complex interplay where Neuromedin U-23 can either directly or indirectly affect pain signaling pathways.

Additionally, Neuromedin U-23 might play a role in stress-induced analgesia, a phenomenon where the body's pain threshold is altered by stress. The neuropeptide's effect on pain perception is thought to be context-dependent, varying with physiological states like stress, inflammation, and injury. Understanding its precise mechanism in these contexts is vital for developing pain management strategies that target Neuromedin U pathways.

The study of Neuromedin U-23 in animal models provides valuable insights into its potential as a target for pain-relief therapies. By exploring its role in pain perception, researchers can identify therapeutic angles to modulate nociceptive signals, offering new avenues for treating chronic pain conditions that do not respond adequately to current treatments. The prospect of modulating Neuromedin U-23 activity to either attenuate or enhance pain responses underscores its importance in pain research and therapy development.

What role does Neuromedin U-23 play in immune system regulation?

Neuromedin U-23 is increasingly being recognized for its role in immune system regulation. This neuropeptide is intertwined with the immune system through its expression and action in various immune cells, indicating its significant involvement in immune responses and inflammation.

Neuromedin U-23's influence on the immune system is evident in its capacity to modulate inflammatory responses. It has been shown to affect the activity of immune cells such as macrophages and lymphocytes, which are key players in the body's defense against infections and injury. By influencing cytokine release, Neuromedin U-23 can alter the inflammatory milieu, impacting both the initiation and resolution of inflammation. For instance, it may enhance the production of pro-inflammatory cytokines like tumor necrosis factor-alpha (TNF-alpha) and interleukins, which facilitate immune cell recruitment and activation.

Moreover, Neuromedin U-23’s interaction with the immune system highlights its role in the neuro-immune axis. This connection is pivotal, as it underscores how neuropeptides like Neuromedin U-23 can serve as a bridge between the nervous and immune systems, facilitating communication and coordination in physiological processes and stress responses.

The regulation of immune responses by Neuromedin U-23 is also linked to its expression under stress conditions. Stress not only impacts neurological functions but also has far-reaching effects on immune activity. Neuromedin U-23's role in mediating stress responses thereby influences immune cell function, potentially affecting an organism's susceptibility to diseases.

Research into NeuroMedin U-23's involvement in immune regulation holds promise for therapeutic applications. By targeting Neuromedin U pathways, it may be possible to modulate immune responses in chronic inflammatory diseases, autoimmunity, and other conditions where immune dysregulation is a hallmark. Understanding the regulatory mechanisms driven by Neuromedin U-23 could lead to the development of drugs that harness its modulatory effects, offering new strategies to treat immune-related disorders.

The exploration of Neuromedin U-23's role in immune function continues to provide deeper insights into the complex dynamics of neuroimmune interactions and their impact on health and disease, indicating its potential as a therapeutic target in immunomodulation.

How is Neuromedin U-23 linked to stress response mechanisms?

Neuromedin U-23 is intricately linked to the body's stress response mechanisms, primarily through its involvement in the hypothalamic-pituitary-adrenal (HPA) axis. This neuropeptide plays a pivotal role in modulating the body's response to stress by influencing neuroendocrine pathways that regulate stress hormone production and secretion.

Under conditions of stress, Neuromedin U-23 expression in the central nervous system, particularly in the hypothalamus, is upregulated. This increase in expression is part of the body's adaptive response to stress, where Neuromedin U-23 helps mediate the release of corticotropin-releasing hormone (CRH). CRH, in turn, stimulates the pituitary gland to secrete adrenocorticotropic hormone (ACTH), which ultimately leads to the release of cortisol from the adrenal cortex. Cortisol is a critical hormone for stress adaptation, influencing metabolism, immune responses, and energy utilization.

Additionally, Neuromedin U-23's role in stress responses extends to behavioral adaptations. It modulates stress-related behaviors such as anxiety and alertness, through interactions with various neuronal circuits and neurotransmitter systems. The peptide's influence on the autonomic nervous system further supports its involvement in stress response, affecting physiological parameters such as heart rate, blood pressure, and gastrointestinal function—typical markers of the stress response.

Moreover, Neuromedin U-23 not only participates in acute stress responses but also influences chronic stress adaptations. Its sustained expression under continuous stress conditions can impact long-term physiological and psychological adaptations, making it a focus in the study of chronic stress-related disorders and mental health conditions such as anxiety and depression.

The research community is actively exploring Neuromedin U-23's potential as a target for modulating stress responses, aiming to develop interventions that could mitigate the adverse effects of stress on health. By understanding the pathways through which Neuromedin U-23 operates, particularly its regulatory effects on the HPA axis and behavioral responses, new strategies can be devised to manage stress-related health issues effectively.

Overall, Neuromedin U-23’s integration in stress response systems highlights its significance in maintaining the balance between homeostasis and adaptability, marking its importance in the broader context of stress physiology and potential therapeutic applications.
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