Everyday more and more scientific breakthroughs in the field of medicine are being reported. These advances in science are undoubtedly very important because of the number of lives that it can potentially save. Just like how stressed and depressed people seek the best psychiatrists to have their mental and emotional states in check, more and more people seek various medicines to sickness that have no cure yet. Below, you will find a selection of studies about the research on L-Carnosine.

Carnosine and anserine as modulators of neutrophil function.

Tan KM, Candlish JK.

Department of Biochemistry, Faculty of Medicine, National University of Singapore, Republic of Singapore. Carnosine and anserine, the bioactive peptides found in most meats and fish, were tested for their ability to modulate neutrophil and U937 cell function, specifically with respect to respiratory burst, interleukin-1 beta production and apoptosis. Both peptides increased the respiratory burst and interleukin-1 beta production of human neutrophils but not of U937 cells. They suppressed apoptosis of human neutrophils but enhanced apoptosis of U937 cells as assessed by DNA strand breaks. These results suggest that carnosine and anserine have the capacity to modulate the immune response at least in human neutrophils.

PMID: 9777271 [PubMed - indexed for MEDLINE]

Possible new antiaging strategies related to neuroendocrine-immune interactions.

Mocchegiani E, Malavolta M.

Immunology Center (Laboratory of Nutrigenomic and Immunosenescence), Research Department INRCA, Ancona, Italy. [email protected]

The aging process demonstrates gradual and spontaneous changes, resulting in maturation through childhood, puberty and young adulthood, and then decline through middle and late age. However, animals and humans are capable of reaching the extreme limit of life span characteristic for the species with a very efficient network of antiaging mechanisms. Among them, neuroendocrine-immune interactions play a pivotal role. The loss of the capacity of the organism in remodeling the neuroendocrine-immune response leads to the appearance of age-associated pathologies. We herein report some substances which can be proposed as new antiaging strategies because of their capacity to remodel some biological functions in old animals and humans. These substances are: L-deprenyl, leptin, ghrelin, carnosine and NO donors. Their role as possible antiaging strategies in healthy people in relation to neuroendocrine-immune responses and zinc ion bioavailability is reported and discussed. Copyright 2008 S. Karger AG, Basel.

PMID: 19047810 [PubMed - indexed for MEDLINE]

Carnosine Protects Against Aβ42-induced Neurotoxicity in Differentiated Rat PC12 Cells

Qiuli Fu1, Haibin Dai1, 2, Weiwei Hu1, Yanying Fan1, Yao Shen1, Weiping Zhang1 and Zhong Chen1

(1) Department of Pharmacology, Institute of Neuroscience, School of Medicine, Zhejiang University, Hangzhou, 310058, China

(2) Department of Pharmacy, Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, 310009, China Received: 11 August 2007 Accepted: 31 October 2007 Published online: 20 November 2007

Abstract (1) The present study was designed to investigate whether histamine is involved in the protective effect of carnosine on Aβ42-induced impairment in differentiated PC12 cells. (2) PC12 cells were exposed to Aβ42 (5 μM) for 24 h after carnosine (5 mM) applied for 18 h. Histamine receptor antagonists (diphenhydramine, zolantidine, thioperamide, clobenpropit) or histidine decarboxylase inhibitor (α-fluoromethylhistidine) were added 15 min before carnosine. Cell viability, glutamate release or cell surface expression of NMDA receptor was examined. (3) Aβ42 caused a concentration-dependent reduction of viability in PC12 cells and pretreatment with carnosine ameliorated this impairment. This amelioration was reversed by the H3 receptor antagonists thioperamide and clobenpropit, but not by either the H1 receptor antagonist diphenhydramine or the H2 receptor antagonist zolantidine. Further, α-fluoromethylhistidine, an irreversible inhibitor of histidine decarboxylase, also had no effect. In the presence of Aβ42, carnosine significantly decreased glutamate release and carnosine increased the surface expression of NMDA receptor. (4) These results indicate that the mechanism by which carnosine attenuates Aβ42-induced neurotoxicity is independent of the carnosine–histidine–histamine pathway, but may act through regulation of glutamate release and NMDA receptor trafficking.

Keywords Carnosine - Alzheimer’s disease - Histamine - Aβ42 - NMDA receptor - Trafficking - Neurotoxicity

Carnosine attenuates mast cell degranulation and histamine release induced by oxygen-glucose deprivation

Yao Shen 1, Shihong Zhang 1, Lin Fu 2, Weiwei Hu 1, Zhong Chen 1 *
1Department of Pharmacology and Neurobiology, School of Medicine, Zhejiang University, Hangzhou, China

2Zhejiang University City College, Hangzhou, China

email: Zhong Chen ([email protected])

*Correspondence to Zhong Chen, Department of Pharmacology, School of Medicine, Zhejiang University, China.

Funded by:

National Natural Science Foundation of China; Grant Number: 30725047, 30572176, 30600757

Zhejiang Province Healthy Excellent Youth Foundation

New Century Excellent Talents Program; Grant Number: NCET-06-0511

Ministry of Education, China

Zhejiang Provincial Scientific Research Foundations; Grant Number: 2006C23025


carnosine • degranulation • histamine • lactate dehydrogenase (LDH) • mast cell • oxygen-glucose deprivation (OGD)


Carnosine (-alanyl-histidine) is a naturally occurring dipeptide that has been characterized as a putative hydrophilic antioxidant. The protective function of carnosine has been demonstrated in neuronal cells under ischemic injury. The purpose of this study was to investigate the effects of carnosine on oxygen-glucose deprivation (OGD)-induced degranulation and histamine release from mast cells. Cultured mast cells were exposed to OGD for 4 h, and then the degranulation was observed immediately by microscopy. Histamine release was analyzed by high-performance liquid chromatography (HPLC). OGD caused degranulation of mast cells, and increased histamine and lactate dehydrogenase (LDH) release. Carnosine (at a concentration of 5 mM) alone did not produce any appreciable effect on degranulation, histamine, and LDH release from mast cells under normal condition, but significantly inhibited the degranulation, histamine, and LDH release of mast cells induced by OGD. These results indicate that carnosine can protect mast cells from degranulation and histamine release and it may be an endogenous mast cell stabilizer in the pathological processes induced by ischemia.

Copyright © 2007 John Wiley & Sons, Ltd.

Received: 12 April 2007; Revised: 1 August 2007; Accepted: 21 August 2007