HTHQ

本公司产品仅用于科研实验，不得用于人体或动物的临床与诊断

HTHQ 是一种对苯二酚单烷基醚，是一种有效的抗氧化剂。

HX-1171, also known as HTHQ, is a lipid peroxidation inhibitor potentially for the treatment of hepatic fibrosis. HTHQ and vitamin E attenuated interleukin-1beta-induced iNOS protein expression in cultured hepatocytes, the potency of HTHQ being 10-times higher than that of vitamin E. HTHQ may prevent tumor production induced by AP and NaNO2 more effectively than ascorbic acid.(In Vitro):HTHQ (0-100 μM; 24 hours; PC12 cells) treatment increases cell viabilities in a dose-dependent manner.HTHQ (10 μM; 0.6-24 hours; PC12 cells) inhibits 3,4-L-Dihydroxyphenylalanine (L-DOPA) -induced phosphorylation of sustaines extracellular signal-regulated kinases (ERK1/2), p38 mitogen-activated protein kinase (MAPK), and c-Jun N-terminal kinase (JNK1/2). HTHQ also normalizes L-DOPA-reduced Bcl-2-associated death protein (Bad) phosphorylation and Bcl-2-associated X protein (Bax) expression, promoting cell survival.(In Vivo):HTHQ (50-200 mg/kg; oral administration; for 4 weeks; specific pathogen-free male Sprague Dawley rats) treatment significantly improves liver weight and serum chemistry level. HTHQ reduces hydroxyproline and malondialdehyde level in the liver. HTHQ treatment also reduces fibrotic septa. HTHQ administration shows reduced mRNA level of PDGF (Plateletderived growth factor) , α-SMA (α-smooth muscle actin) and TGF-β (transforming growth factor-β) than DMN-induced hepetic fibrosis animals in the liver tissue.

HTHQ (0-100 μM; 24 hours; PC12 cells) treatment increases cell viabilities in a dose-dependent manner.HTHQ (10 μM; 0.6-24 hours; PC12 cells) inhibits 3,4-L-Dihydroxyphenylalanine (L-DOPA) -induced phosphorylation of sustaines extracellular signal-regulated kinases (ERK1/2), p38 mitogen-activated protein kinase (MAPK), and c-Jun N-terminal kinase (JNK1/2). HTHQ also normalizes L-DOPA-reduced Bcl-2-associated death protein (Bad) phosphorylation and Bcl-2-associated X protein (Bax) expression, promoting cell survival. Cell Viability Assay Cell Line:PC12 cells Concentration:0 μM, 1 μM, 10 μM, and 100 μM Incubation Time:24 hours Result:Reduced cell viability at 24 hours caused by both 100 and 200 μM L-DOPA was significantly attenuated.Western Blot Analysis Cell Line:PC12 cells Concentration:10 μM Incubation Time:0.6-24 hours Result:Inhibited L-DOPA-induced phosphorylation of sustained extracellular signal-regulated kinases (ERK1/2), p38 mitogen-activated protein kinase (MAPK), and c-Jun N-terminal kinase (JNK1/2). And also normalized L-DOPA-reduced Bcl-2-associated death protein (Bad) phosphorylation and Bcl-2-associated X protein (Bax) expression.

HTHQ (50-200 mg/kg; oral administration; for 4 weeks; specific pathogen-free male Sprague Dawley rats) treatment significantly improves liver weight and serum chemistry level. HTHQ reduces hydroxyproline and malondialdehyde level in the liver. HTHQ treatment also reduces fibrotic septa. HTHQ administration shows reduced mRNA level of PDGF (Plateletderived growth factor) , α-SMA (α-smooth muscle actin) and TGF-β (transforming growth factor-β) than DMN-induced hepetic fibrosis animals in the liver tissue. Animal Model:48 specific pathogen-free male Sprague Dawley (SD) rats (6-week-old ) with dimethylnitrosamine (DMN) Dosage:50 mg/kg, 100 mg/kg, 200 mg/kg Administration:Oral administration; for 4 weeks Result:Improved against DMN-induced liver fibrosis in male SD rats.

HX-1171 | HX-1171 | HX-1171 | HTHQ

Others

Other Targets

Others

Others-Field

——

148081-72-5

236.35

C15H24O2

>98% (HPLC)

DMSO : ≥ 100 mg/mL; 423.10 mM

CCCCCCOc1c(c(c(c(c1)C)O)C)C

4-(hexyloxy)-2,3,6-trimethylphenol

(-20℃)

With Ice Pack

≥ 2 years