scholarly journals α-Melanocyte-Stimulating Hormone and Related Tripeptides: Biochemistry, Antiinflammatory and Protective Effects in Vitro and in Vivo, and Future Perspectives for the Treatment of Immune-Mediated Inflammatory Diseases

2008 ◽  
Vol 29 (5) ◽  
pp. 581-602 ◽  
Author(s):  
Thomas Brzoska ◽  
Thomas A. Luger ◽  
Christian Maaser ◽  
Christoph Abels ◽  
Markus Böhm
Keyword(s):  
Inflammatory Diseases ◽  
Protective Effects ◽  
Future Perspectives ◽  
Melanocyte Stimulating Hormone ◽  
Immune Mediated ◽  
Stimulating Hormone

scholarly journals α-Melanocyte Stimulating Hormone Prevents Lipopolysaccharide-Induced Vasculitis by Down-Regulating Endothelial Cell Adhesion Molecule Expression

Endocrinology ◽  
2003 ◽  
Vol 144 (1) ◽  
pp. 360-370 ◽  
Author(s):  
T. E. Scholzen ◽  
C. Sunderkötter ◽  
D.-H. Kalden ◽  
T. Brzoska ◽  
M. Fastrich ◽  
...  
Keyword(s):  
Cell Adhesion ◽  
Inflammatory Diseases ◽  
Nuclear Factor Κb ◽  
Vascular Damage ◽  
Adhesion Assay ◽  
Melanocyte Stimulating Hormone ◽  
And Function ◽  
Stimulating Hormone

Abstract The neuroendocrine hormone α-melanocyte stimulating hormone (MSH) has profound antiinflammatory and immunomodulating properties. Here we have examined the possibility that α-MSH may interfere with the expression and function of cell adhesion molecules (CAMs) expressed by human dermal microvascular endothelial cells (HDMECs) in response to lipopolysaccharide (LPS) or TNFα in vitro and in vivo. In HDMEC, α-MSH (10−8/10−12m) profoundly reduced the mRNA and protein expression of E-selectin, vascular CAM (VCAM)-1, and intercellular CAM (ICAM)-1 induced by LPS or TNFα as determined by semiquantitative RT-PCR, ELISA, and fluorescence-activated cell sorter analysis. In addition, α-MSH significantly impaired the LPS-induced ICAM-1 and VCAM-1-mediated adhesion of lymphocytes to HDMEC monolayer in a functional adhesion assay. Likewise, α-MSH effectively inhibited the transcription factor nuclear factor-κB activation in HDMEC, which is required for CAM gene expression. Importantly in vivo, in murine LPS-induced cutaneous vasculitis (local Shwartzman reaction), a single ip injection of α-MSH significantly suppressed the deleterious vascular damage and hemorrhage by inhibiting the sustained expression of vascular E-selectin and VCAM-1. This persistent expression has been implicated in the dysregulation of diapedesis and activation of leukocytes, which subsequently leads to hemorrhagic vascular damage. Our findings indicate that α-MSH may have an important therapeutical potential for the treatment of vasculitis, sepsis, and inflammatory diseases.

scholarly journals TRPM8 Deficiency Attenuates Liver Fibrosis Through S100A9-HNF4α Signaling

2022 ◽  
Author(s):  
Qiang Liu ◽  
Xiaohua Lei ◽  
Zhenyu Cao ◽  
Ju Zhang ◽  
Likun Yan ◽  
...  
Keyword(s):  
Liver Fibrosis ◽  
Transient Receptor Potential ◽  
Inflammatory Diseases ◽  
Receptor Potential ◽  
Potential Effect ◽  
Protective Effects ◽  
Tissue Samples ◽  
Duct Ligation

Abstract Background Liver fibrosis represent a major global health care burden. Data emerging from recent advances have suggested TRPM8, a member of the transient receptor potential (TRP) family of ion channels, plays an essential role in various chronic inflammatory diseases. However, its role in liver fibrosis remains unknown. Herein, we assessed the potential effect of TRPM8 in liver fibrosis. Methods The effect of TRPM8 was evaluated using specimens obtained from classic murine models of liver fibrosis, namely wild-type (WT) and TRPM8−/− (KO) fibrotic mice after carbon tetrachloride (CCl4) or bile duct ligation (BDL) treatment. The role of TRPM8 was systematically evaluated using specimens obtained from the aforementioned animal models after various in vivo and in vitro experiments. Results Clinicopathological analysis has shown TRPM8 expression was upregulated in tissue samples from cirrhosis patients and fibrotic mice. TRPM8 deficiency not only attenuated inflammation and fibrosis progression in mice, but also helped to alleviate symptoms of cholangiopathies. Moreover, reduction in S100A9 and increase in HNF4α expressions were observed in liver of CCl4 and BDL treated TRPM8 KO mice. Strong regulatory linkage between S100A9 and HNF4α was also noticed in L02 cells underwent siRNA-mediated S100A9 knockdown and S100A9 overexpressing plasmid transfection. Lastly, alleviative effect of a selective TRPM8 antagonist was confirmed in vivo. Conclusion These findings suggest TRPM8 deficiency may exert protective effects against inflammation, cholangiopathies and fibrosis through S100A9-HNF4α signaling mechanistically. M8-B might be a promising therapeutic candidate for liver fibrosis.

Effects of different opiate agonists on melanocyte-stimulating hormone release: in vivo and in vitro studies

1980 ◽  
Vol 58 (3) ◽  
pp. 326-329 ◽  
Author(s):  
M. E. Celis
Keyword(s):  
Opioid Peptides ◽  
In Vitro Studies ◽  
Hormone Release ◽  
Low Concentration ◽  
Melanocyte Stimulating Hormone ◽  
Dose Dependent ◽  
Stimulating Hormone

The effects of Leu-enkephalin, Met-enkephalin, and β-endorphin on melanocyte-stimulating hormone (MSH) secretion were studied in vivo and in vitro. The three opioid peptides release MSH. In vitro this release is dose dependent for Met-enkephalin between 10 and 1000 ng/mL and for Leu-enkephalin between 10 and 100 ng/mL. β-Endorphin releases MSH at the low concentration of 1 ng/mL and the effect is dose dependent between 1 and 100 ng/mL. Naloxone reverses this effect. In vivo the three petptides release MSH.

Three types of alpha-melanocyte-stimulating hormone: bioactivities and half-lives

1983 ◽  
Vol 245 (1) ◽  
pp. E47-E54 ◽  
Author(s):  
D. Rudman ◽  
B. M. Hollins ◽  
M. H. Kutner ◽  
S. D. Moffitt ◽  
M. J. Lynn
Keyword(s):  
Tissue Slices ◽  
Melanocyte Stimulating Hormone ◽  
Lipolytic Action ◽  
Acetyl Group ◽  
Isolated Adipocytes ◽  
Hydroxy Groups ◽  
Kinetics Of ◽  
Stimulating Hormone

Three types of alpha-melanocyte-stimulating hormone (alpha MSH) that differ in the acetyl status of the N-terminal serine have been found in the neurointermediate lobe of the pituitary gland and in the brain: desacetyl alpha MSH, which lacks an acetyl group; monoacetyl alpha MSH, in which the amino group of the serine is acetylated; and diacetyl alpha MSH, in which both amino and hydroxy groups of the serine are acetylated. We compared the lipolytic and melanotropic actions of these three peptides, and their rates of disappearance from plasma, both in vitro and in vivo. The following differences were found. a) For in vitro lipolytic actions on rabbit adipose tissue slices, the potencies differed according to the order diacetyl = monoacetyl greater than desacetyl. On rabbit isolated adipocytes, however, the three peptides were equipotent. b) For in vivo lipolytic action in the rabbit, not only potency but also kinetics differed. Diacetyl alpha MSH had the slowest onset, longest duration, and greatest potency. The desacetyl variant had the quickest onset, shortest duration, and least potency. c) The half-life for elimination from rabbit plasma both in vitro and in vivo was shortest for the desacetyl form and longest for the diacetyl peptide. d) For in vitro melanotropic effect on frog skin, kinetics of action were the same for all three peptides, but potency differed according to the order diacetyl = monoacetyl greater than desacetyl. Thus acetylation of alpha MSH alters lipolytic and melanotropic potencies in vitro and lipolytic potency and kinetics in vivo. These differences result in part from the fact that acetylation slows the degradation of the tridecapeptide both inside and outside the circulation.

MELANOCYTE STIMULATING HORMONE INHIBITION BY ACETYLCHOLINE AND NORADRENALINE IN THE FROG SKIN BIOASSAY

1966 ◽  
Vol 51 (1) ◽  
pp. 149-160 ◽  
Author(s):  
Halvor Möller ◽  
Aaron B. Lerner
Keyword(s):  
Frog Skin ◽  
Rana Pipiens ◽  
Individual Response ◽  
Melanocyte Stimulating Hormone ◽  
Skin Samples ◽  
Stimulating Hormone

ABSTRACT The mechanism of aggregation induced in MSH-dispersed dermal melanocytes was studied in Rana pipiens by reflectance photometry in vitro and by microscopy in vivo. Acetylcholine inhibits MSH strongly and irreversibly in one third of all frogs tested in vitro and has almost no effect on the remaining animals. No lightening action occurs in vivo. Different skin samples from the same animal give the same response to acetylcholine. An individual response to acetylcholine implies similar responses to other cholinergics. The lightening action of acetylcholine is inhibited by atropine. Noradrenaline induces a reversible MSH-inhibition in all frogs in vitro as well as in vivo. The lightening action of noradrenaline, inhibited by sympatholytics, is ten times stronger than that of acetylcholine. The l-isomer has only twice the lightening potency as the d-isomer. Both lightening agents work if given at the maximum of MSH-dispersion or before the addition of MSH. Fundamental differences between the mechanisms of dispersion and aggregation, and between the lightening induced by acetylcholine and by noradrenaline, are emphasized.

Melanocyte-stimulating Hormone Activity of Synthetic MSH and ACTH Peptides, in vivo and in vitro

Nature ◽  
1965 ◽  
Vol 207 (5000) ◽  
pp. 978-979 ◽  
Author(s):  
ABBA J. KASTIN ◽  
ANDREW V. SCHALLY ◽  
HARUAKI YAJIMA ◽  
KAZUO KUBO
Keyword(s):  
Hormone Activity ◽  
Melanocyte Stimulating Hormone ◽  
Stimulating Hormone

Endogenous ACTH, not only α-melanocyte-stimulating hormone, reduces food intake mediated by hypothalamic mechanisms

2010 ◽  
Vol 298 (2) ◽  
pp. E237-E244 ◽  
Author(s):  
Carla Schulz ◽  
Kerstin Paulus ◽  
Ralf Lobmann ◽  
Mary Dallman ◽  
Hendrik Lehnert
Keyword(s):  
Food Intake ◽  
Body Weight Gain ◽  
Reduce Food Intake ◽  
Melanocyte Stimulating Hormone ◽  
Paraventricular Nuclei ◽  
Close Proximity ◽  
Robust Evidence ◽  
Stimulating Hormone

ACTH and α-melanocyte-stimulating hormone (α-MSH) are both consecutively processed from proopiomelanocortin (POMC), which is synthesized in hypothalamic arcuate neurons innervating the paraventricular nuclei (PVN). POMC secretion/synthesis is regulated by energy availability. ACTH and α-MSH bind with equal affinity to melanocortin-4 receptors and elicit similar effects on signal transduction in-vitro. Endogenous α-MSH thus far is believed to be the major physiological agonist and to act in an anorexigenic manner. Until now, it was fully unknown whether endogenous ACTH is also involved in the regulation of appetite and food intake. In this study in rats, we now show that icv ACTH as well as α-MSH possess anorexigenic effects in the PVN or areas in close proximity in vivo and that the effect of ACTH is direct and not mediated via α-MSH. We investigated the roles of endogenous ACTH and α-MSH by PVN application of the respective antibodies under different physiological conditions. In satiated rats with high levels of ACTH and α-MSH in the PVN, antibody administration increased food intake and body weight gain; hungry animals were unaffected. Finally, repeated injections of ACTH antibodies into PVN resulted in persistently increased food intake during the light period. These data now provide robust evidence that endogenous ACTH without further processing acts in the PVN or areas in close proximity to reduce food intake under conditions of feeding-induced satiety.

scholarly journals Mechanistic Perspectives of Maslinic Acid in Targeting Inflammation

2015 ◽  
Vol 2015 ◽  
pp. 1-9 ◽  
Author(s):  
Wei Hsum Yap ◽  
Yang Mooi Lim
Keyword(s):  
Arachidonic Acid ◽  
Inflammatory Diseases ◽  
Experimental Models ◽  
Arachidonic Acid Metabolism ◽  
Protective Effects ◽  
Pentacyclic Triterpene ◽  
Maslinic Acid ◽  
Anti Inflammatory

Chronic inflammation drives the development of various pathological diseases such as rheumatoid arthritis, atherosclerosis, multiple sclerosis, and cancer. The arachidonic acid pathway represents one of the major mechanisms for inflammation. Prostaglandins (PGs) are lipid products generated from arachidonic acid by the action of cyclooxygenase (COX) enzymes and their activity is blocked by nonsteroidal anti-inflammatory drugs (NSAIDS). The use of natural compounds in regulation of COX activity/prostaglandins production is receiving increasing attention. In Mediterranean diet, olive oil and table olives contain significant dietary sources of maslinic acid. Maslinic acid is arising as a safe and novel natural pentacyclic triterpene which has protective effects against chronic inflammatory diseases in variousin vivoandin vitroexperimental models. Understanding the anti-inflammatory mechanism of maslinic acid is crucial for its development as a potential dietary nutraceutical. This review focuses on the mechanistic action of maslinic acid in regulating the inflammation pathways through modulation of the arachidonic acid metabolism including the nuclear factor-kappa B (NF-κB)/COX-2 expression, upstream protein kinase signaling, and phospholipase A2enzyme activity. Further investigations may provide insight into the mechanism of maslinic acid in regulating the molecular targets and their associated pathways in response to specific inflammatory stimuli.

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