Protective Effect of Baicalin Against Carbon Tetrachloride-Induced Acute Hepatic Injury in Mice

This study examined the effects of baicalin, a bioactive flavonoid isolated from Scutellariae Radix, on carbon tetrachloride (CCl4)-induced liver injury. Mice were treated intraperitoneally with 0.5 ml/kg CCl4and different groups of animals received 25, 50, 100, and 200 mg/kg baicalin. At 24 h after...

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Main Authors: Sang-Won Park (Author), Chan-Ho Lee (Author), Yeong Shik Kim (Author), Sam Sik Kang (Author), Su Jin Jeon (Author), Kun Ho Son (Author), Sun-Mee Lee (Author)
Format: Book
Published: Elsevier, 2008-01-01T00:00:00Z.
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100 1 0 |a Sang-Won Park  |e author 
700 1 0 |a Chan-Ho Lee  |e author 
700 1 0 |a Yeong Shik Kim  |e author 
700 1 0 |a Sam Sik Kang  |e author 
700 1 0 |a Su Jin Jeon  |e author 
700 1 0 |a Kun Ho Son  |e author 
700 1 0 |a Sun-Mee Lee  |e author 
245 0 0 |a Protective Effect of Baicalin Against Carbon Tetrachloride-Induced Acute Hepatic Injury in Mice 
260 |b Elsevier,   |c 2008-01-01T00:00:00Z. 
500 |a 1347-8613 
500 |a 10.1254/jphs.FP0071392 
520 |a This study examined the effects of baicalin, a bioactive flavonoid isolated from Scutellariae Radix, on carbon tetrachloride (CCl4)-induced liver injury. Mice were treated intraperitoneally with 0.5 ml/kg CCl4and different groups of animals received 25, 50, 100, and 200 mg/kg baicalin. At 24 h after the CCl4treatment, the level of serum aminotransferases and lipid peroxidation was significantly elevated, whereas the hepatic glutathione content was decreased. These changes were attenuated by baicalin. The histological studies showed that baicalin inhibited the portal inflammation, centrizonal necrosis, and Kupffer cell hyperplasia, which are the three most common characteristics of CCl4-induced liver damage. The serum level and mRNA expression of tumor necrosis factor-α were markedly increased by the CCl4treatment but suppressed by baicalin. The mRNA and protein expression levels of inducible nitric oxide synthase and heme oxygenase-1 increased significantly at 24 h after the CCl4treatment. Baicalin attenuated the increase in the protein and gene expression of inducible nitric oxide synthase but augmented the increase in those of heme oxygenase-1. These findings suggest that baicalin protects hepatocytes from the oxidative damage caused by CCl4, and this protection is likely due to the induction of HO-1 expression and the inhibition of the proinflammatory mediators. Keywords:: baicalin, carbon tetrachloride (CCl4), heme oxygenase-1, oxidative stress, xyhproinflammatory mediator 
546 |a EN 
690 |a Therapeutics. Pharmacology 
690 |a RM1-950 
655 7 |a article  |2 local 
786 0 |n Journal of Pharmacological Sciences, Vol 106, Iss 1, Pp 136-143 (2008) 
787 0 |n http://www.sciencedirect.com/science/article/pii/S1347861319315464 
787 0 |n https://doaj.org/toc/1347-8613 
856 4 1 |u https://doaj.org/article/a5874f9628e347cc91aebb5ea6df929a  |z Connect to this object online.