15 results on '"Guzmán-Mejía F"'
Search Results
2. Role of main neuroendocrine pathways activated by swim stress on mast cell-dependent peritoneal TNF production after LPS administration in mice
- Author
-
Romero-Carbente, J. C., Guzmán-Mejía, F., Cruz, S. L., López-Rubalcava, C., and González-Espinosa, C.
- Published
- 2014
- Full Text
- View/download PDF
3. Stimulation of nAchRα7 Receptor Inhibits TNF Synthesis and Secretion in Response to LPS Treatment of Mast Cells by Targeting ERK1/2 and TACE Activation.
- Author
-
Guzmán-Mejía, F., López-Rubalcava, C., and González-Espinosa, C.
- Abstract
The cholinergic anti-inflammatory pathway is recognized as one of the main mechanisms of neuromodulation of the immune system. Activation of the α7 nicotinic acetylcholine receptor (nAchRα7) suppresses cytokine synthesis in distinct immune cells but the molecular mechanisms behind this effect remain to be fully described. Mast cells (MCs) are essential players of allergic reactions and innate immunity responses related to chronic inflammation. Activation of TLR4 receptor in MCs leads to the rapid secretion of pre-synthesized TNF from intracellular pools and to the activation of NFκB, necessary for de novo synthesis of TNF and other cytokines. Here we report that the nAchRα7 receptor specific agonist GTS-21 inhibits TLR4-induced secretion of preformed TNF from MCs in vivo and in vitro
. Utilizing bone marrow-derived mast cells (BMMCs) it was found that GTS-21 also diminished secretion of de novo synthesized TNF, TNF mRNA accumulation and IKK-dependent p65-NFκB phosphorylation in response to LPS. nAchRα7 triggering prevented TLR4-induced ERK1/2 phosphorylation, which resulted an essential step for TNF secretion due to the phosphorylation of the metallopeptidase responsible for TNF maturation (TACE). Main inhibitory actions of GTS-21 were prevented by AG490, an inhibitor of JAK-2 kinase. Our results show for the first time, that besides the prevention of NFκB-dependent transcription, inhibitory actions of nAchRα7 triggering include the blockade of pathways leading to exocytosis of granule-stored cytokines in MCs. [ABSTRACT FROM AUTHOR]- Published
- 2018
- Full Text
- View/download PDF
4. Looking Inside of the Intestinal Permeability Regulation by Protein-Derivatives from Bovine Milk.
- Author
-
Guzmán-Mejía F, Molotla-Torres DE, Godínez-Victoria M, Valdes-Hilarios X, Sánchez-Miranda E, Oros-Pantoja R, and Drago-Serrano ME
- Subjects
- Animals, Humans, Cattle, Colostrum chemistry, Milk chemistry, Intestinal Absorption drug effects, Tight Junction Proteins metabolism, Intestinal Barrier Function, Permeability, Intestinal Mucosa metabolism, Intestinal Mucosa drug effects, Milk Proteins pharmacology, Milk Proteins chemistry
- Abstract
The prime function of the epithelium is to regulate the intestinal permeability; the latter is a quantitative parameter that refers to the measurement of the rate of passage of solutes through the epithelial monolayer. Function of epithelial monolayer depends on the expression of protein complexes known as tight junction proteins; whose function and expression can be disrupted under conditions of inflammation including irritable bowel disease (IBD), intestinal infections, and high-fat diets, among others. This manuscript is focused to outline the effects of bovine milk protein derivatives on the intestinal permeability addressed mostly in animal models in which the intestinal barrier is disrupted. At present, the properties of bovine milk protein derivatives on intestinal permeability have been scarcely documented in humans, but evidence raised from clinical trials provides promising findings of potential application of colostrum to control of the intestinal permeability in critically ill patients, users of non-steroid anti-inflammatory drugs, like athletes and militia members., (© 2024 The Author(s). Molecular Nutrition & Food Research published by Wiley‐VCH GmbH.)
- Published
- 2024
- Full Text
- View/download PDF
5. Moderate Aerobic Exercise Induces Homeostatic IgA Generation in Senile Mice.
- Author
-
Hernández-Urbán AJ, Drago-Serrano ME, Reséndiz-Albor AA, Sierra-Ramírez JA, Guzmán-Mejía F, Oros-Pantoja R, and Godínez-Victoria M
- Subjects
- Animals, Mice, Cytokines metabolism, B-Lymphocytes immunology, B-Lymphocytes metabolism, B-Cell Activating Factor metabolism, B-Cell Activating Factor genetics, Intestinal Mucosa metabolism, Intestinal Mucosa immunology, Intestine, Small immunology, Intestine, Small metabolism, Male, Plasma Cells immunology, Plasma Cells metabolism, Tumor Necrosis Factor Ligand Superfamily Member 13 metabolism, Tumor Necrosis Factor Ligand Superfamily Member 13 genetics, Physical Conditioning, Animal, Immunoglobulin A metabolism, Immunoglobulin A immunology, Mice, Inbred BALB C, Aging immunology, Homeostasis
- Abstract
A T-cell-independent (TI) pathway activated by microbiota results in the generation of low-affinity homeostatic IgA with a critical role in intestinal homeostasis. Moderate aerobic exercise (MAE) provides a beneficial impact on intestinal immunity, but the action of MAE on TI-IgA generation under senescence conditions is unknown. This study aimed to determine the effects of long-term MAE on TI-IgA production in young (3 month old) BALB/c mice exercised until adulthood (6 months) or aging (24 months). Lamina propria (LP) from the small intestine was obtained to determine B cell and plasma cell sub-populations by flow cytometry and molecular factors related to class switch recombination [Thymic Stromal Lymphopoietin (TSLP), A Proliferation-Inducing Ligand (APRIL), B Cell Activating Factor (BAFF), inducible nitric oxide synthase (iNOS), and retinal dehydrogenase (RDH)] and the synthesis of IgA [α-chain, interleukin (IL)-6, IL-21, and Growth Factor-β (TGF-β)]; and epithelial cells evaluated IgA transitosis [polymeric immunoglobulin receptor (pIgR), tumor necrosis factor-α (TNF-α), interferon-γ (IFN-γ), IL-4] by the RT-qPCR technique. The results were compared with data obtained from sedentary age-matched mice. Statistical analysis was computed with ANOVA, and p < 0.05 was considered to be a statistically significant difference. Under senescence conditions, MAE promoted the B cell and IgA+ B cells and APRIL, which may improve the intestinal response and ameliorate the inflammatory environment associated presumably with the downmodulation of pro-inflammatory mediators involved in the upmodulation of pIgR expression. Data suggested that MAE improved IgA and downmodulate the cytokine pro-inflammatory expression favoring homeostatic conditions in aging.
- Published
- 2024
- Full Text
- View/download PDF
6. Effect of chronic stress on gel-forming mucins in the small intestine of BALB/c mice.
- Author
-
Gutiérrez-Galicia JK, Drago-Serrano ME, Oros-Pantoja R, Godínez-Victoria M, and Guzmán-Mejía F
- Subjects
- Animals, Female, Mice, Stress, Psychological metabolism, Stress, Psychological immunology, Interleukin-18 metabolism, Mucin 5AC metabolism, Stress, Physiological, Immunoglobulin A metabolism, Mucin-2 metabolism, Mucin-2 genetics, Mice, Inbred BALB C, Intestine, Small metabolism, Intestine, Small microbiology, Intestine, Small pathology, Goblet Cells metabolism, Goblet Cells pathology, Mucins metabolism
- Abstract
Intestinal homeostasis involves the collaboration of gut barrier components, such as goblet cells and IgA-microbiota complexes, that are under the control of stress that promotes inflammatory responses addressed primarily in the colon. The aim of this study was to evaluate the effect of stress on mucins, goblet cells, and proinflammatory parameters in the proximal and distal regions of the small intestine. A group ( n = 6) of female 8-week-old BALB/c mice underwent board immobilization stress (2 h per day for 4 days) and were sacrificed with isoflurane. Samples from proximal and distal small segments were collected to analyze the following: 1) goblet cells stained with periodic acid-Schiff (PAS) and with alcian blue (AB) to visualize histologically neutral and acidic mucins, respectively; 2) IgA-microbiota complexes identified by flow cytometry in intestinal lavages; and 3) MUC2, MUC5AC , and IL-18 mRNA levels in whole mucosal scrapings by reverse transcription-qPCR. Regarding the unstressed group, in the proximal region of small intestine both PAS+ and AB+ goblet cells were unchanged; however, MUC5AC and IL-18 mRNA levels were increased, and the percentage of IgA-microbiota complexes was reduced. In the distal segment, the number of PAS+ goblet cells was increased, whereas the number of AB+ goblet cells was reduced and did not affect the remaining parameters. The data suggest that stress induces inflammation in the proximal small intestine; these findings may provide an experimental reference for human diseases that may affect the proximal small intestine, such as Crohn's disease, in which stress contributes to the progression of intestinal inflammation or relapse., Competing Interests: The authors declare no conflict of interest., (© 2024 by the authors.)
- Published
- 2024
- Full Text
- View/download PDF
7. Outcome of stress on G protein-coupled receptors and hypoxia inducible factor-1α.
- Author
-
Reséndiz-Albor AA, Arciniega-Martínez IM, Montes de Oca AC, Guzmán-Mejía F, Drago-Serrano ME, Estrada-Jiménez T, and Abarca-Rojano E
- Subjects
- Animals, Mice, Stress, Psychological metabolism, Male, Colon metabolism, Intestinal Mucosa metabolism, Receptors, G-Protein-Coupled metabolism, Hypoxia-Inducible Factor 1, alpha Subunit metabolism, Mice, Inbred BALB C
- Abstract
Stress drives neuroendocrine signals with detrimental effects to the intestinal homeostasis. The aim of this study was to evaluate the effect of stress on intestinal hypoxia response elements, including G protein-coupled receptor 41 (GPR41), GPR43, and hypoxia inducible factor (HIF)-1α. Groups of five BALB/c mice were subjected to acute (2 h per day) and chronic (2 h per day for 4 days) stress induced by restraint, and the results were compared to those of an unstressed control group. Whole mucosal samples from the colon were collected to evaluate the expression of GPR41, GPR43 and HIF-1α using Western blot chemiluminescent analysis. Compared to the control group, in the chronic stress group the expression of GPR43 ( P = 0.0092) and HIF-1α ( P < 0.0001) were significantly lower and the expression of GPR41 was similar ( P = 0.9184); acute stress significantly increased HIF-1α expression ( P = 0.0030) and increased GPR41 expression ( P = 0.0937), without affecting GPR43 ( P = 0.9184). These findings offer insights into the modulation of hypoxia response elements under stress conditions and their pharmacological implications for developing drugs that mitigate the effects of stress on intestinal homeostasis., Competing Interests: The authors declare no conflict of interest., (© 2024 by the authors.)
- Published
- 2024
- Full Text
- View/download PDF
8. Exercise improves intestinal IgA production by T-dependent cell pathway in adults but not in aged mice.
- Author
-
Hernández-Urbán AJ, Drago-Serrano ME, Cruz-Baquero A, García-Hernández AL, Arciniega-Martínez IM, Pacheco-Yépez J, Guzmán-Mejía F, and Godínez-Victoria M
- Subjects
- Humans, Mice, Animals, Adult, Infant, Interleukin-10, Intestines, RNA, Messenger, T-Lymphocytes, Immunoglobulin A genetics
- Abstract
Introduction: Hypermutated high-affinity immunoglobulin A (IgA), neutralizes toxins and drives the diversification of bacteria communities to maintain intestinal homeostasis although the mechanism underlies the impact of moderate aerobic exercise (MAE) on the IgA-generation via T-dependent (TD) is not fully know. Therefore, the aim of this study was to determine the effect of long-time MAE on the production of IgA through the TD pathway in Peyer´s patches of the small intestine from aged mice., Methods: MAE protocol consisted of twenty 3-month-old (young) BALB/c mice running in an endless band at 0° inclination and a speed of 10 m/h for 5 days a week and resting 2 days on the weekend until reaching 6-month-old (adulthood, n=10) or 24-month-old (aging, n=10). Groups of young, adult, or elderly mice were included as sedentary controls (n=10/per group). At 6 or 24 months old, all were sacrificed, and small intestine samples were dissected to prepare intestinal lavages for IgA quantitation by ELISA and to obtain suspensions from Peyer´s patches (PP) and lamina propria (LP) cells for analysis of T, B, and plasma cell subpopulations by flow cytometry and mRNA analysis expression by RT-qPCR of molecular factors related to differentiation of B cells to IgA+ plasma cells, class switch recombination, and IgA-synthesis. Statistical analysis was computed with two-way ANOVA (factor A=age, factor B=group) and p<0.05 was considered for statistically significant differences., Results: Compared to age-matched sedentary control, in exercised elderly mice, parameters were either increased (IgA concentration, IL-21, IL-10 and RDH mRNA expression), decreased (α-chain mRNA, B cells, mIgA+ B cells, mIgM+ B cells and IL-4 mRNA) or unchanged (PP mIgA+ plasmablasts and LP cyt-IgA+ plasma cells). Regarding the exercised adult mice, they showed an up-modulation of IgA-concentration, mRNA expression IL-21, IL-10, and RDH and cells (PP B and T cells, mIgM+ plasmablasts and LP cyt-IgA+plasma cells)., Conclusion: Our findings suggest that MAE restored the IgA production in adult mice via the TD cell pathway but does not in aged mice. Other studies are necessary to know in more detail the impact of long-time MAE on the TD pathway to produce IgA in aging., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2023 Hernández-Urbán, Drago-Serrano, Cruz-Baquero, García-Hernández, Arciniega-Martínez, Pacheco-Yépez, Guzmán-Mejía and Godínez-Victoria.)
- Published
- 2023
- Full Text
- View/download PDF
9. Regionalized analysis of gut barrier components in the small intestine of BALB/c mice following chronic immobilization stress.
- Author
-
Guzmán-Mejía F, Godínez-Victoria M, García-Hernández AL, Gutierrez-Galicia JK, Molotla Torres DE, and Drago-Serrano ME
- Subjects
- Female, Animals, Mice, Mice, Inbred BALB C, Interleukin-6 metabolism, Tight Junction Proteins genetics, Tight Junction Proteins metabolism, RNA, Messenger genetics, Albumins metabolism, Albumins pharmacology, Intestinal Mucosa, Cytokines metabolism, Intestine, Small metabolism
- Abstract
Background: Microbiota and tight junction proteins (TJPs) are components of the gut barrier, and are considered stress targets that have deleterious effects on intestinal homeostasis., Objectives: This study aimed to evaluate the effects of chronic immobilization stress on selected small intestine homeostasis parameters., Material and Methods: Female BALB/c mice were divided into a stress group that underwent short-term immobilization for 2 h per day for 4 consecutive days, and a non-stressed control group (n = 6 per group). Proximal and distal small intestine samples were excised to assess colony-forming units per gram (CFU/g) of total bifidobacteria in selective agar plates, luminal albumin was assessed using immune-enzymatic assay, pro-inflammatory cytokines were evaluated using reverse transcription-quantitative polymerase chain reaction (RT-qPCR), and TJPs (pore-forming, claudin (Cld)-2; pore-sealing, Cld-4; ambiguous, Cld-7, -12 and -15) were assessed with RT-qPCR and western blotting., Results: Compared with the control group, the stress group had lower body weight and energy intake. In the distal region, the stressed mice had lower bifidobacteria count and messenger ribonucleic acid (mRNA) expression of Cld-2, Cld-4 and Cld-12, though they had more albumin and higher interleukin (IL)-6 mRNA expression. Within the proximal region, the stressed mice had higher mRNA expression of tumor necrosis factor alpha (TNF-α), interferon gamma (IFN-γ), IL-6, Cld-7, Cld-12, and Cld-15, along with lower levels of IL-10 and Cld-4. However, mRNA and protein expression of TJPs were discordant., Conclusions: These findings indicate divergent stress-induced outcomes in the small intestine, evidenced by the elicitation of a pro-inflammatory response and decreased anti-inflammatory response in the duodenum, and by increased albumin transudation and decreased bifidobacterial growth in the distal region.
- Published
- 2023
- Full Text
- View/download PDF
10. Role of Stress on Driving the Intestinal Paracellular Permeability.
- Author
-
Molotla-Torres DE, Guzmán-Mejía F, Godínez-Victoria M, and Drago-Serrano ME
- Abstract
The gut epithelium is a polarized monolayer that exhibits apical and basolateral membrane surfaces. Monolayer cell components are joined side by side via protein complexes known as tight junction proteins (TJPs), expressed at the most apical extreme of the basolateral membrane. The gut epithelium is a physical barrier that determinates intestinal permeability, referred to as the measurement of the transit of molecules from the intestinal lumen to the bloodstream or, conversely, from the blood to the gut lumen. TJPs play a role in the control of intestinal permeability that can be disrupted by stress through signal pathways triggered by the ligation of receptors with stress hormones like glucocorticoids. Preclinical studies conducted under in vitro and/or in vivo conditions have addressed underlying mechanisms that account for the impact of stress on gut permeability. These mechanisms may provide insights for novel therapeutic interventions in diseases in which stress is a risk factor, like irritable bowel syndrome. The focus of this study was to review, in an integrative context, the neuroendocrine effects of stress, with special emphasis on TJPs along with intestinal permeability.
- Published
- 2023
- Full Text
- View/download PDF
11. Lactoferrin as a Component of Pharmaceutical Preparations: An Experimental Focus.
- Author
-
Guzmán-Mejía F, Godínez-Victoria M, Molotla-Torres DE, and Drago-Serrano ME
- Abstract
Lactoferrin is an 80 kDa monomeric glycoprotein that exhibits multitask activities. Lactoferrin properties are of interest in the pharmaceutical field for the design of products with therapeutic potential, including nanoparticles and liposomes, among many others. In antimicrobial preparations, lactoferrin has been included either as a main bioactive component or as an enhancer of the activity and potency of first-line antibiotics. In some proposals based on nanoparticles, lactoferrin has been included in delivery systems to transport and protect drugs from enzymatic degradation in the intestine, favoring the bioavailability for the treatment of inflammatory bowel disease and colon cancer. Moreover, nanoparticles loaded with lactoferrin have been formulated as delivery systems to transport drugs for neurodegenerative diseases, which cannot cross the blood-brain barrier to enter the central nervous system. This manuscript is focused on pharmaceutical products either containing lactoferrin as the bioactive component or formulated with lactoferrin as the carrier considering its interaction with receptors expressed in tissues as targets of drugs delivered via parenteral or mucosal administration. We hope that this manuscript provides insights about the therapeutic possibilities of pharmaceutical Lf preparations with a sustainable approach that contributes to decreasing the resistance of antimicrobials and enhancing the bioavailability of first-line drugs for intestinal chronic inflammation and neurodegenerative diseases.
- Published
- 2023
- Full Text
- View/download PDF
12. Cholecystokinin Outcome on Markers of Intestinal IgA Antibody Response.
- Author
-
Morales-Magaña J, Arciniega-Martínez IM, Drago-Serrano ME, Reséndiz-Albor AA, Jarillo-Luna RA, Cruz-Baquero A, Gómez-López M, Guzmán-Mejía F, and Pacheco-Yépez J
- Abstract
Cholecystokinin 8 (CCK8) is an entero-octapeptide that participates in crosstalk with components of intestinal immunity via the CCK receptor (CCKR), but its role in modulation of the IgA response is not fully known under physiological conditions. Male eight-week-old BALB/c mice each were intraperitoneally injected once during 7 days with CCK8, devazapide (CCKR1 antagonist), L365,260 (CCKR2 antagonist) or vehicle (sham group). In intestinal lavages, total and secretory IgA (SIgA) were determined by ELISA; in lamina propria, IgA
+ B lymphocytes and IgA+ plasma cells were analyzed by flow cytometry; mRNA levels of polymeric immunoglobulin receptor (pIgR) in epithelial cells and α chain, interleukins (ILs) in lamina propria cells were assessed by qRTPCR. Regarding the sham conditions, IgA+ plasma-cell percentage and IL-2, IL-5, IL-10 and transforming growth factor-β (TGF-β) mRNA levels were either increased by CCK8 or decreased by both CCKR antagonists. For IgA/SIgA responses, IL-4/IL-6 mRNA levels were decreased by all drugs and pIgR mRNA was increased by CCK8 and reduced by L365,260. IgA+ B cell percentage and α chain mRNA levels were elicited by CCK8 and L365,260. Data suggested a presumable differential role of CCK/CCKR on the IgA-response; outcome of L365,260 on the elicitation of IgA+ B cells and α chain mRNA needs further examination.- Published
- 2022
- Full Text
- View/download PDF
13. Lactoferrin and Its Potential Impact for the Relief of Pain: A Preclinical Approach.
- Author
-
Godínez-Chaparro B, Guzmán-Mejía F, and Drago-Serrano ME
- Abstract
Pain is one of the most disabling symptoms of several clinical conditions. Neurobiologically, it is classified as nociceptive, inflammatory, neuropathic and dysfunctional. Opioids and nonsteroidal anti-inflammatory drugs (NSAIDs) are conventionally prescribed for the treatment of pain. Long-term administration of opioids results in the loss of analgesic efficacy, leading to increased dosage, tolerance, and addiction as the main drawbacks of their use, while the adverse effects of NSAIDs include gastric ulcer formation, intestinal bleeding, acute kidney injury, and hepatotoxicity. Lactoferrin is an iron-binding, anti-inflammatory glycoprotein that displays analgesic activities associated, in part, by interacting with the low-density lipoprotein receptor-related protein (LRP), which may result in the regulation of the DAMP-TRAF6-NFκB, NO-cGMP-ATP K
+ -sensitive channel and opioid receptor signaling pathways. This review summarizes and discusses for the first time the analgesic effects of lactoferrin and its presumable mechanisms based on pre-clinical trials. Given its anti-nociceptive and anti-inflammatory properties, lactoferrin may be used as an adjunct to enhance the efficacy and to decrease the tolerogenic effects of canonical therapeutic drugs prescribed for pain treatment.- Published
- 2021
- Full Text
- View/download PDF
14. Intestinal Homeostasis under Stress Siege.
- Author
-
Guzmán-Mejía F, Godínez-Victoria M, Vega-Bautista A, Pacheco-Yépez J, and Drago-Serrano ME
- Subjects
- Animals, Homeostasis, Humans, Mucus immunology, Immunoglobulin G metabolism, Intestinal Mucosa immunology, Stress, Psychological immunology
- Abstract
Intestinal homeostasis encompasses a complex and balanced interplay among a wide array of components that collaborate to maintain gut barrier integrity. The appropriate function of the gut barrier requires the mucus layer, a sticky cushion of mucopolysaccharides that overlays the epithelial cell surface. Mucus plays a critical anti-inflammatory role by preventing direct contact between luminal microbiota and the surface of the epithelial cell monolayer. Moreover, mucus is enriched with pivotal effectors of intestinal immunity, such as immunoglobulin A (IgA). A fragile and delicate equilibrium that supports proper barrier function can be disturbed by stress. The impact of stress upon intestinal homeostasis results from neuroendocrine mediators of the brain-gut axis (BGA), which comprises a nervous branch that includes the enteric nervous system (ENS) and the sympathetic and parasympathetic nervous systems, as well as an endocrine branch of the hypothalamic-pituitary-adrenal axis. This review is the first to discuss the experimental animal models that address the impact of stress on components of intestinal homeostasis, with special emphasis on intestinal mucus and IgA. Basic knowledge from animal models provides the foundations of pharmacologic and immunological interventions to control disturbances associated with conditions that are exacerbated by emotional stress, such as irritable bowel syndrome.
- Published
- 2021
- Full Text
- View/download PDF
15. Bovine lactoferrin as a Modulator of Neuroendocrine Components of Stress.
- Author
-
Guzmán-Mejía F, Vega-Bautista A, Molotla-Torres DE, Aguirre-Garrido JF, and Drago-Serrano ME
- Subjects
- Hypothalamo-Hypophyseal System metabolism, Neurosecretory Systems metabolism, Pituitary-Adrenal System metabolism, Lactoferrin metabolism, Stress, Physiological
- Abstract
Stress is a condition that maintains the homeostasis of the organism through the activation of different neuroendocrine pathways and secretion of a wide array of chemical mediators, including corticotropin-releasing hormone (CRH), neurotransmitters and glucocorticoids hormones. These molecules fulfill important physiological functions, but under stressful conditions, they can induce or aggravate a pathological state depending on type, severity and duration of stress. For this reason, the search for compounds that modulate the activity of the neuroendocrine pathways is crucial for the control of diseases associated with stressful situations. Bovine lactoferrin (bLf) is an iron-binding multifunctional glycoprotein that exhibits modulatory properties on the neuroendocrine system. Bovine lactoferrin affects the production and secretion of neuroendocrine components of the hypothalamus-pituitary-adrenal (HPA) axis. Neuroendocrine mechanisms of bLf entail either the down- or up-modulation of adrenal corticosteroids via HPA pathway activation, nitric oxide (NO) generation and opioid nervous system pathway activation. This manuscript is focused on reviewing the current contributions of bLf modulatory actions on the response of hormones, neurotransmitters involved in stress and behavior. Sustained use of drugs for stress-associated dysfunctions loses efficacy and requires the dose increase by tolerance and drug dependence. Therefore, bLf may be included as a therapeutic and/or adjunctive agent of drugbased therapies for the treatment of stress-associated emotional-disturbances., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)
- Published
- 2021
- Full Text
- View/download PDF
Catalog
Discovery Service for Jio Institute Digital Library
For full access to our library's resources, please sign in.