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MedChemExpressModel D(+)-Galactosamine hydrochloride -1772-03-8

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D(+)-Galactosamine (D-Galactosamine) hydrochloride, which is an established experimental toxin, primarily causes liver injury by the generation of free radicals and depletion of UTP nucleotides. D(+)-Galactosamine hydrochloride intoxication also induces renal dysfunction thus, renal failure is often associated with the end-stage of the liver damage. Lipopolysaccharide/D(+)-Galactosamine-induced acute liver injury is a known animal model of fulminant hepatic failure[1][2].
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D(+)-Galactosamine hydrochloride

MCE China:D(+)-Galactosamine hydrochloride

Brand:MedChemExpress (MCE)

Cat. No.HY-42682

CAS:1772-03-8

Synonyms:D-Galactosamine HCl

Purity:98.0%

Storage:4°C, sealed storage, away from moisture *In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture)

Shipping:Room temperature in continental US; may vary elsewhere.

Description:D(+)-Galactosamine (D-Galactosamine) hydrochloride, which is an established experimental toxin, primarily causes liver injury by the generation of free radicals and depletion of UTP nucleotides. D(+)-Galactosamine hydrochloride intoxication also induces renal dysfunction thus, renal failure is often associated with the end-stage of the liver damage. Lipopolysaccharide/D(+)-Galactosamine-induced acute liver injury is a known animal model of fulminant hepatic failure.

In Vitro:D(+)-Galactosamine (5 mM, 0-24 h) hydrochloride induces apoptosis and necrosis in primary culture of rat hepatocytes, and induces caspase-3 activation and DNA fragmentation[3].

In Vivo:D-Galactosamine can be used to induce hepatitis models. .f12{ font-size: 12px; } .fwb{ font-weight: bold; } .lh22{ line-height: 22px;; } .lh23 { line-height: 23px; } .pl13{ padding-left: 13px;; } .part { margin-top: 18px; } .mold-first-tit { width: 100%; height: 44px; line-height: 44px; background: #F9F7FB; border-bottom: 1px solid #EBE4F6; padding-left: 16px; box-sizing: border-box; margin-bottom: 17px; } .mold-second-tit:before { content:""; width: 6px; height: 6px; display: inline-block; border-radius: 50%; background: rgba(255,102,0,0.4); margin-right: 12px; position: relative; top: -3px; } .lft-border { border-left: 1px dotted #EBE4F6; padding-right: 12px; margin-left: 3px; box-sizing: border-box; padding-bottom: 12px; } /* .part .dec:last-child { border-bottom: 0; } */ .dec { margin: 10px 15px 0; padding-bottom: 10px; border-bottom: 1px dashed #EBE4F6; } .btm-border { border-left: 1px dashed #EBE4F6; } .text-bg { margin-top: 10px; background: #FFFBF1; padding: 14px; border-bottom: 0; position: relative; } .text-note-bg { margin-top: 10px; background: #FFFDF7; padding: 12px; border-bottom: 0; position: relative; } .text-note { width: 51px; height: 20px; line-height: 20px; background: #FFE2AA; text-align: center; border-radius: 0 0 8px 0; position: absolute; top: 0; left: 0; } .text-note-dec { margin-top: 15px;; } Induction of Hepatitis Background D-Galactosamine-induced hepatotoxicity is similar to viral hepatitis. D-Galactosamine induces the lipids peroxidation and thus leads to deterioration of cell membrane[5]. Specific Mmodeling Methods Rat: Wistar • 110-180 g • femaleAdministration: 250 mg/kg • i.p. • 6 injection in 24 hours or 1.5 g/kg • i.p. • single dose Note For 250 mg/kg, 6 injections: first 3 of injections with 4 hours intervals, after 14 hours pause, the last 3 of injections with 1 hour intervals. Modeling Indicators Molecular changes: Increased bilirubin, hemoglobin, and enzyme activities of GOT, GPT and GIDH in serum. Depleted glycogen from hepatocytes. Decreased levels of adenine nucleotides and UDP-glucose in liver metabolite. Decreased serum proteins and prothrombin activity.Morphology: Decreased weight and consistency of liver.Hemorrhages in several organs, particularly in gut and stomach.Histological Analysis: Induced necrosis and inflammatory infiltration in periportal areas, induced appearance of councilman bodies, enlarged and increased kupffer cells. Correlated Product(s): Lipopolysaccharide (HY-D1056) Opposite Product(s): Bergenin (HY-N0017); Glycyrrhizin (HY-N0184); Bicyclol (HY-B0766); Chrysin (HY-14589)

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References:

[1]. Li Y, et al. Inhibition of PI3K/AKt/mTOR signaling pathway protects against d-galactosamine/lipopolysaccharide-induced acute liver failure by chaperone-mediated autophagy in rats. Biomed Pharmacother. 2017 Aug;92:544-553.  [Content Brief]

[2]. Liu Y, et al. AMSC-derived exosomes alleviate lipopolysaccharide/d-galactosamine-induced acute liver failure by miR-17-mediated reduction of TXNIP/NLRP3 inflammasome activation in macrophages. EBioMedicine. 2018 Oct;36:140-150.  [Content Brief]

[3]. Siendones E, et al. PGE1 abolishes the mitochondrial-independent cell death pathway induced by D-galactosamine in primary culture of rat hepatocytes. J Gastroenterol Hepatol. 2005 Jan;20(1):108-16.  [Content Brief]

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