Ala-Gly
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Ala-Gly

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Category
Others
Catalog number
BAT-015414
CAS number
687-69-4
Molecular Formula
C5H10N2O3
Molecular Weight
146.14
Ala-Gly
IUPAC Name
2-[[(2S)-2-aminopropanoyl]amino]acetic acid
Synonyms
(S)-2-(2-Aminopropanamido)acetic acid; L-Alanyl-glycine; N-L-Alanylglycine
Purity
95%
Density
1.263 g/cm3
Melting Point
249-255°C (dec.)
Boiling Point
417.4°C at 760 mmHg
Sequence
H-Ala-Gly-OH
Storage
Store at -20°C
InChI
InChI=1S/C5H10N2O3/c1-3(6)5(10)7-2-4(8)9/h3H,2,6H2,1H3,(H,7,10)(H,8,9)/t3-/m0/s1
InChI Key
CXISPYVYMQWFLE-VKHMYHEASA-N
Canonical SMILES
CC(C(=O)NCC(=O)O)N
1. Mechanism of Ser-Ala-Gly-Pro-Ala-Phe treatment with a pulsed electric field to improve ethanol-induced gastric mucosa injury in mice
Liangzi Sun, Mengqi Li, Shuyu Zhang, Zhijie Bao, Songyi Lin Food Funct. 2022 Jun 20;13(12):6716-6725. doi: 10.1039/d2fo00567k.
This paper focused on the mechanism of Ser-Ala-Gly-Pro-Ala-Phe (SAGPAF) treatment to improve gastric mucosal injury in mice. A gastric mucosa injury model induced by ethanol was established, and the superoxide dismutase (SOD) activity, malondialdehyde (MDA) content, nitric oxide (NO) content and myeloperoxidase (MPO) level were determined. We performed macroscopic and histopathological evaluation of the gastric organs. Moreover, we analyzed the mechanism of SAGPAF treatment by western blotting. Compared with the model group, the SOD activity and NO content in the medium-dose and high-dose SAGPAF groups of treated with 10 kV cm-1 field intensity were significantly increased. The MDA content and MPO level were decreased significantly. They significantly reduced the gastric mucosal injury induced by ethanol (21.17 ± 3.51% and 13.99 ± 2.00%) and the histopathological scores (3.83 ± 0.40 and 4.33 ± 0.37) (P < 0.05). Western blotting analysis showed that SAGPAF after pulsed electric field (PEF) treatment improved gastric injury by reducing protein phosphorylation. These findings provided strong evidence that PEF-treated SAGPAF enhanced the gastric mucosal barrier function by inhibiting the activation of the mitogen-activated protein kinase (MAPK) and nuclear factor kappa-B (NF-κB) signaling pathways, reducing the ethanol-induced inflammatory response and oxidative stress.
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