α-Melanocyte stimulating hormone has beneficial effects on cerulein-induced acute pancreatitis

Jahovic, Nermina; Arbak, Serap; Tekeli, Seçkin Özgür; Ali̇can, İnci̇

doi:10.1016/j.peptides.2003.11.008

Cited by 15 publications

(9 citation statements)

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“…The peptide also improves disease characteristics in a model of murine colitis by inhibiting colonic NO production (Rajora et al, 1997). Moreover, our previous observations revealed that α-MSH is beneficial in endotoxin-induced ileitis (San et al, 2001) and cerulein-induced acute pancreatitis models in rats (Jahovic et al, 2004) and protects the gastric tissue against 75% ethanol (unpublished observation).…”

Section: Discussionmentioning

confidence: 82%

The effect of α‐melanocyte stimulating hormone on gentamicin‐induced acute nephrotoxicity in rats

Kolgazi

Arbak

Ali̇can

2007

J of Applied Toxicology

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The effect of alpha-melanocyte stimulating hormone (alpha-MSH) was investigated on gentamicin-induced acute renal injury in rats. Sprague-Dawley rats (200-250 g; n = 8-10) were treated with gentamicin sulphate (GEN; 80 mg kg(-1)) or saline intraperitoneally for 7 consecutive days. alpha-MSH was administered at a dose of 25 microg rat(-1) day(-1) following GEN or saline injections. On day 8, all animals were decapitated. Trunk blood and 24 h urine were collected to measure the serum creatinine levels, blood urea nitrogen (BUN) levels and to calculate the creatinine clearance values. The kidneys were excised for histological evaluation and for the measurement of malondialdehyde (MDA) levels, glutathione (GSH) contents and myeloperoxidase (MPO) activity. Treatment with alpha-MSH reduced the severity of the renal lesions microscopically, decreased MDA content and MPO activity and restored GSH in kidney samples. However, it did not restore the impaired renal function tests due to GEN challenge. In conclusion, alpha-MSH treatment has a beneficial effect on GEN-induced acute nephrotoxicity, as confirmed by histological evaluation and biochemical assays; but it does not improve GEN-induced renal dysfunction. The mechanism of the protective effect could be attributed, at least in part, to decreased tissue leukocyte infiltration and thus, to decreased oxygen-derived reactive metabolite production.

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Section: Discussionmentioning

confidence: 82%

The effect of α‐melanocyte stimulating hormone on gentamicin‐induced acute nephrotoxicity in rats

Kolgazi

Arbak

Ali̇can

2007

J of Applied Toxicology

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“…Therapeutic α-MSH-treatments have been tried in animal models of septic shock, contact dermatitis, rheumatoid arthritis, acute pancreatitis, toxin-induced liver failure, allergic airway inflammation, endotoxin induce uveitis, and experimental autoimmune uveoretinitis (Ceriani et al, 1994;Grabbe et al, 1996;Jahovic et al, 2004;Martin and Lipton, 1990;Nishida et al, 2004;Raap et al, 2003;Shiratori et al, 2004;Taylor et al, 2000;Wang et al, 2004). In addition, two other groups of researchers have attempted to use different forms of gene therapy to see if delivering α-MSH into the immune response of EAE will suppress the onset and subsequent pathology of EAE.…”

Section: Discussionmentioning

confidence: 99%

The diminishment of experimental autoimmune encephalomyelitis (EAE) by neuropeptide alpha-melanocyte stimulating hormone (α-MSH) therapy

Taylor

Kitaichi

2008

Brain, Behavior, and Immunity

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The neuropeptide alpha-melanocyte stimulating hormone (α-MSH) plays an important role in immune privilege by its suppression of inflammation, and its induction of regulatory T cells. This finding led us to test the possibility that we can use α-MSH to suppress autoimmune diseases, and promote re-establishment of immune tolerance to autoantigens. To test this possibility, SJL mice with experimental autoimmune encephalomyelitis (EAE) were injected with α-MSH at the first signs of paralysis. The α-MSH-treated mice in comparison with untreated EAE mice had a profound diminishment in the severity and tempo of EAE. The spleen cells in α-MSH-treated EAE produced TGF-β in response to PLP-antigen stimulation in contrast to untreated mice spleen cells that produced IFN-γ. When the α-MSH-treated EAE mice were reimmunized there was a delay of a week before the second episode of EAE. Although this delay maybe because of the induction of TGF-β-producing spleen cells by the α-MSH-treatment, it was not adequate to suppress IFN-γ-production by PLP-antigen stimulated spleen cells from untreated mice, nor able to suppress the eventual second episode of EAE. Therefore, the injection of α-MSH at the onset of paralysis is extremely effective in diminishing the severity and tempo of EAE, and the subsequent induction of potential PLP-specific Treg cells suggests that an α-MSH therapy could be attempted as part of a therapeutic regiment to impose immunoregulation and immunosuppression on an autoimmune disease of the central nervous system.

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“…In vivo studies have revealed systemic and organ-specific anti-inflammatory functions of a-MSH (40). a-MSH suppressed pyrogen-induced fever; counteracted organ fibrosis by reducing expression of collagen type-1; quenched allergic airway and ocular inflammation, and by mechanisms not completely elucidated, attenuated pancreatic inflammation (78)(79)(80)(81)(82). Systemic or subcutaneous injection of a-MSH decreased circulating levels of IL-1a and TNF-a and improved the survival rates of mice used as models of peritonitis/endotoxaemia (82,83).…”

Section: Melanocortins and Other Melanogenesis-related Proteins Have mentioning

confidence: 99%

Melanin and melanogenesis in adipose tissue: possible mechanisms for abating oxidative stress and inflammation?

Page¹,

Chandhoke²,

Baranova³

2011

Obesity Reviews

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SummaryObesity has become a worldwide epidemic and can lead to multiple chronic diseases. Adipose tissue is increasingly thought to play an active role in obesityrelated pathologies such as insulin resistance and non-alcoholic fatty liver disease. Obesity has been strongly associated with systemic inflammation and, to a lesser degree, with oxidative stress, although the causal relationships among these factors are unclear. A recent study demonstrating an expression of the components of the melanogenic pathway and the presence of melanin in visceral adipose has raised questions regarding the possible role of melanogenesis in adipose tissue. As this study also found larger amounts of melanin in the adipose tissue of obese patients relative to lean ones, we hypothesize that melanin, a pigment known for its antioxidant and anti-inflammatory properties, may scavenge reactive oxygen species and abate oxidative stress and inflammation in adipose tissue. This review considers the evidence to support such a hypothesis, and speculates on the role of melanin within adipocytes. Furthermore, we consider whether the a-melanocytestimulating hormone or its synthetic analogues could be used to stimulate melanin production in adipocytes, should the hypothesis be supported in future experiments.

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α-Melanocyte stimulating hormone has beneficial effects on cerulein-induced acute pancreatitis

Cited by 15 publications

References 15 publications

The effect of α‐melanocyte stimulating hormone on gentamicin‐induced acute nephrotoxicity in rats

The effect of α‐melanocyte stimulating hormone on gentamicin‐induced acute nephrotoxicity in rats

The diminishment of experimental autoimmune encephalomyelitis (EAE) by neuropeptide alpha-melanocyte stimulating hormone (α-MSH) therapy

Melanin and melanogenesis in adipose tissue: possible mechanisms for abating oxidative stress and inflammation?

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