Effects of α-lipoic acid and L-carnosine supplementation on antioxidant activities and lipid profiles in rats

Kim, Mi Young; Kim, Eun Jin; Kim, Young Nam; Choi, Changsun; Lee, Bog‐Hieu

doi:10.4162/nrp.2011.5.5.421

Cited by 62 publications

(48 citation statements)

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“…Alpha-lipoic acid (ALA), chemically named 5-(1,2-dithiolan-3-yl) pentanoic acid (C 8 H 14 O 2 S 2 ), is a naturally occurring compound which is found in plants and animals and functions as anti-oxygen in virtually all body tissues [35,36]. In humans, ALA is mainly synthesized in tissues with highly metabolic activities like the liver, kidney, and heart [37]. ALA, which is traditionally known as one of the requisite cofactors in mitochondrial respiratory enzymes, is capable of scavenging reactive oxygen species and free radicals to keep the redox homeostasis in the cells and recycling endogenous antioxidants like Vitamin C, Vitamin E, and GSH [38][39][40].…”

Section: Discussionmentioning

confidence: 99%

Apoptotic events induced by high glucose in human hepatoma HepG2 cells involve endoplasmic reticulum stress and MAPK’s activation

et al. 2014

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To investigate whether endoplasmic reticulum (ER) stress participates in the induction of apoptosis in HepG2 cells exposed to high glucose and explore its probable mechanism. A series of experiments were performed following HepG2 cells treated with different concentrations of glucose for 48 h. The apoptosis was detected by means of Hoechst staining and flow cytometry. Caspase-3 activity assay was performed by measuring the pNA (p-nitroaniline) to indirectly reveal the catalytic activity of caspase-3. The expression levels of apoptosis-, ER stress-associated proteins and MAPKs were analyzed by western blot. To further characterize the molecular mechanisms, the effects of antioxidant alpha-lipoic acid (ALA) and specific inhibitors for JNK and p38 (SP600125 and SB203580, respectively) were examined by Hoechst staining, immunofluorescence, and western blot. After HepG2 cells were incubated with high glucose for 48 h, both Hoechst staining and flow cytometry analyses unveiled the apoptosis of HepG2 cells. Caspase-3 activity assay revealed that the activity of caspase-3 was enhanced. Western blot showed an enhancement of pro-caspase-9 degradation, a reduction of Bcl-2/Bax ratio, a decrease in GRP78 expression, and increases in CHOP and p47/phox levels. In addition, western blot analysis presented that phosphorylation of p38 and JNK was triggered and that the expression of ASK1 was elevated. In the case of the contributions of oxidative stress and the MAPK signaling pathways, all ALA, SP600125 and SB203580 were able to largely rescue high glucose-induced apoptosis. High glucose induced the apoptosis in HepG2 cells through the activation of ASK1-p38/JNK pathway mediated by ER stress and oxidative stress.

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Section: Discussionmentioning

confidence: 99%

Apoptotic events induced by high glucose in human hepatoma HepG2 cells involve endoplasmic reticulum stress and MAPK’s activation

et al. 2014

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“…Alpha-Lipoic acid is a substance with antioxidant properties that easily penetrates the skin as a result of its lipid soluble characteristics as well as its low molecular weight (Beitner 2003). According to Kim et al (2011), Freisleben et al (1994) observed that topical α-lipoic acid cream applied to hairless mice penetrates the epidermis and is distributed in the dermis and the subcutaneous tissue after 4 h. This revelation and the fact that enhanced protection of human cells against ultraviolet light by antioxidant combinations involving dietary carotenoids has been earlier observed are suggestive of the role of UVB on tissue damage exhibited by sun-exposed animals.…”

Section: Discussionmentioning

confidence: 99%

An investigation of the cause of death in Wistar rats exposed to sunlight: focus on tissue histology

Iyanda

Oparinde

2014

International Journal of Biological Research

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Objective: The aim of the study is to investigate the effects of ultraviolet rays of the sun on organs like the liver, brain, heart, kidney, lung and ileum. Methods: Fourteen female rats (235 g) were used for the study and equally distributed into 2 groups. While the rats in the test groups were left in an open place for a period of 7 hours daily for adequate exposure to sunlight, control rats were kept in cages at ambient temperature of 26°C in the animal house. When all the animals died on the 10th day of study, samples of different tissues were obtained, fixed in 10% neutral buffered formalin and stained with hematoxylin and eosin (H & E). Results: 100% mortality was recorded. Results showed no visible lesion for all the tissues of control rats whereas pathological features like severe congestion of the coronary vessel and mild pulmonary congestion as well as thickening of alveolar wall were reported for heart and lung respectively in sun-exposed rats. Moreover, in sun-exposed rats other tissues such as the brain, ileum, kidney and liver showed no visible lesion. Conclusion: From the outcome of this study, it may be inferred that excessive sun exposure can be a cause of mortality in a nocturnal animal species, with death resulting from multi-organ damage.

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“…3 The N-terminal part is a fragment of galanin (2)(3)(4)(5)(6)(7)(8)(9)(10)(11)(12)(13) and the C-terminal part is the other bioactive dipeptide L-carnosine capable of scavenging hydroxyl radicals (Table 1). 6 A fragment of galanin (2)(3)(4)(5)(6)(7)(8)(9)(10)(11)(12)(13) contains residues Trp, 2 Asn, 5 Gly 8 and Tyr, 9 which are necessary for interaction of the peptide with the GalR2 receptor 7,8 and thereby to trigger cardioprotective effects. L-carnosine tailing to C-terminal part of peptide G1 enhances its resistance to the action of exopeptidases due to the insertion of βAla14.…”

Section: Structure and Properties F Of Peptide G1mentioning

confidence: 99%

“…Post-ischaemic administration of the peptides improved functional recovery of isolated perfused rat hearts and reduced infarct size in rats in vivo. 4,5 The chimeric ligand [βAla14, His15]-galanin (2-15) (G1), which is composed of galanin (2)(3)(4)(5)(6)(7)(8)(9)(10)(11)(12)(13) and the dipeptide carnosine, exhibited the most beneficial effect. 3 The mechanisms of action of peptide G1 remain unclear.…”

mentioning

confidence: 99%

Galanin receptors activation modulates myocardial metabolic and antioxidant responses to ischaemia/reperfusion stress

Студнева

Serebryakova

Veselova

et al. 2019

Clin Exp Pharma Physio

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The neuropeptide galanin comprising 29 amino acid residues (30 in humans) is widely expressed in the central nervous system and peripheral organs and tissues. Galanin exerts its biological activities through three different G protein-coupled receptors, GalR1, GalR2 and GalR3, all of which are found in the heart. 1 Over the past decade, a wealth of data has been accumulated that substantiates targeting galanin receptors for the treatment of various human diseases and pathological conditions, including Alzheimer's disease, metabolic diseases, mood disorders, pain, anxiety and solid tumors. 2 However, the physiological and pharmacological effects of galanin in heart diseases are much less studied. We have recently demonstrated that N-terminal fragments of galanin (2-11) and(2-15) and their chemically modified analogues reduce experimental myocardial I/R injury. 3-5 These peptides increased cell viability, AbstractThe mechanisms of protective action of the neuropeptide galanin and its N-terminal fragments against myocardial ischaemia/reperfusion (I/R) injury remain obscure. The aim of this work was to study effects of a novel peptide agonist of galanin receptors [βAla14, His15]-galanin (2-15) (G1) and the full-length galanin (G2) on energy and antioxidant status of the heart with acute infarction. The peptides were synthesized by the automatic solid phase method using Fmoc technology. Their structure was identified by 1 H-NMR spectroscopy and MALDI-TOF mass spectrometry. Experiments were performed on anaesthetized open-chest rats subjected to myocardial regional ischaemia and reperfusion. Intravenous (iv) administration of optimal doses of peptides G1 and G2 (1.0 and 0.5 mg/kg, respectively, at the onset of reperfusion significantly reduced infarct size (on average by 40% compared with control) and the plasma activity of creatine kinase-MB (CK-MB) and lactate dehydrogenase (LDH).These effects were associated with augmented preservation of aerobic energy metabolism, increased activity of Cu,Zn superoxide dismutase (Cu,Zn-SOD), catalase (CAT) and glutathione peroxidase (GSH-Px) and decreased lipid peroxidation in the area at risk (AAR) at the end of reperfusion. Peptide G1 showed more efficient recovery of the majority of metabolic and antioxidant parameters. The results provide evidence that the galaninergic system can be considered a promising target to reduce energy dysregulation and oxidative damage in myocardial I/R injury. K E Y W O R D Santioxidant defence, energy metabolism, galanin, myocardial infarction, necrosis markers, rat

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Effects of α-lipoic acid and L-carnosine supplementation on antioxidant activities and lipid profiles in rats

Cited by 62 publications

References 50 publications

Apoptotic events induced by high glucose in human hepatoma HepG2 cells involve endoplasmic reticulum stress and MAPK’s activation

Apoptotic events induced by high glucose in human hepatoma HepG2 cells involve endoplasmic reticulum stress and MAPK’s activation

An investigation of the cause of death in Wistar rats exposed to sunlight: focus on tissue histology

Galanin receptors activation modulates myocardial metabolic and antioxidant responses to ischaemia/reperfusion stress

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