Search

In the case of alcoholic liver injury, an iron overload is always present. Both alcohol and iron can individually induce oxidative stress in liver. However, the combined effect of physiological concentrations of alcohol and iron on oxidative stress in hepatocytes remains unknown. Baicalin has been demonstrated to be an antioxidant or iron chelator in animal experiments. In this study, we investigated the injury to hepatocytes CYP2E1-independently induced by the combination of alcohol and iron and the protective effect of baicalin. Compared with cells treated with ethanol alone, ferric citrate enhanced the accumulation of reactive oxygen and nitrogen species, increased the occurrence of protein carbonylation/nitration and the levels of 4-hydroxy-2-nonenal, changed the distribution of iNOS, and eventually resulted in apoptosis. However, pretreatment with baicalin inhibited the oxidative stress induced by the combination of alcohol and iron, mainly by chelating iron. Our findings therefore suggest that iron could CPY2E1-independently enhance the oxidative stress induced by alcohol, which probably contributes to the pathogenesis of alcoholic liver disease. Baicalin is a promising phytomedicine for preventing alcoholic liver disease., (Copyright © 2012 Elsevier Ltd. All rights reserved.)

Baicalin has been reported to protect against liver injury in iron-overload mice, however, the mechanisms underlying the hepatoprotective properties of baicalin are poorly understood. In this study, we systematically studied the protective effect of baicalin on iron overload induced liver injury, as well as the underlying mechanism based on nitrative stress in rat model. We found that when iron overload rats (500mgiron/kg) were fed baicalin-containing diet (0.3% and 1% w/w) for 45days, baicalin dose dependently protected against iron overload induced liver injury, including alleviation of hepatic pathological damage, decrease of SOD activity, iron content, carbonyl content, and the thiobarbituric acid-reactive substances level in hepatic tissues. It also increased serum iron content, SH content and GPx activity, decreased serum ALT and AST activities. Immunohistochemistry and immunoprecipitation analysis revealed that baicalin could also inhibit iron overload induced protein tyrosine nitration in liver. Moreover, in iron overload rat liver, we found that baicalin decreased the iron overload increased level of glutathione-S-transferases (GSTs) expression, oxidation and nitration. These results suggest that not only oxidative stress, but also nitrative stress, is involved in iron overload induced liver injury, and the underlying mechanism might partially relate to the involvement of GSTs expression and post-translational modification. Baicalin can effectively prevent iron overload caused abnormality and can be a candidate medicine for iron overload diseases., (Copyright © 2012 Elsevier B.V. All rights reserved.)

Hemin-nitrite-H2O2 system may play a role in liver oxidative injury in some pathological events. In this paper, the effects of the three active components of the root of Scutellaria baicalensis Georgi, i.e. baicalin, baicalein and wogonin, on hemin-nitrite-H2O2 induced liver injury were studied in liver homogenate, liver microsome and human hepatoblastoma cell line HepG2 cells. It was found that hemin-nitrite-H2O2 could induce liver homogenate protein nitration, lipid peroxidation and liver microsome protein oxidation; it also caused a decrease of HepG2 cells viability. Baicalein, baicalin and wogonin could inhibit protein nitration and lipid peroxidation in liver homogenate as well as in HepG2 cells in a dose-dependent manner, the inhibition order was baicalein>baicalin>>wogonin. These three flavonoids also inhibited the oxidation of protein in liver microsome, the decrease of cell viability and the content of GSH in HepG2 cells, among which baicalin represented the most inhibitory effect. Besides, hemin-H2O2 induced cell injury could be augmented with the existence of nitrite, indicating protein nitration involved in hemin-nitrite-H2O2 induced liver injury. These results demonstrated hemin-nitrite-H2O2 could induce liver injury through oxidizing or nitrating different biomolecules. Baicalein, baicalin and wogonin could inhibit hemin-nitrite-H2O2 induced liver injury in dose-dependent manners by inhibiting oxidation and nitration.

The introduction of new iron chelating drugs may ultimately improve iron-chelation therapy for patients with iron overload diseases such as thalassaemia and other disorders. In this paper, the in vivo effects of baicalin and quercetin on iron overload induced liver injury were studied on mice. It was found that when iron-dextran induced iron overload mice were fed baicalin or quercetin containing diet (1% w/w) for 45 days, both flavonoids significantly inhibited iron overload induced lipid peroxidation and protein oxidation of liver, decreased hepatic iron and hepatic collagen content, increased the serum non-heme iron level but not serum ferritin level. Flavonoids supplementation also increased the excretion of iron through feces. In vitro study demonstrated that both flavonoids could release iron from ferritin. These results indicate that besides acting as antioxidants, both flavonoids can also release iron from liver and finally excrete it through feces. The present study provides further support for flavonoids to be medicines for iron overload diseases.

Iron overload is one of the most common metal related toxicity. Under this circumstance, excessive iron deposition in liver will lead to further injury such as hepatocellular necrosis, inflammation, fibrosis, and in some cases even to carcinoma. In this paper, the effect of a nature flavonoid, baicalin, on iron overload-induced mouse liver oxidative injury has been studied. It was found that when iron-dextran-induced iron overload, mice were fed baicalin-containing diet (0.25% and 1%) for 50 days, hepatic iron, liver-to-body weight ratio, and hepatic lipid peroxidation were dose-dependently decreased; while catalase activity, total antioxidant status, and serum iron content were dose dependently increased. The protective effect of baicalin on liver of iron overload mouse may due to both the antioxidant and iron chelation activities of baicalin. These data provide preliminary experimental support for baicalin as medicine for iron overload diseases.

Oxidative injury has been implicated in the pathogenesis of numerous neurodegenerative diseases. Recently, it has been found that with the existence of hydrogen peroxide and nitrite, hemin catalyzes protein nitration. We hypothesize under certain pathological conditions, hemin catalyzed protein nitration may happen in the brain. In this paper, the effects of three flavonoids, i.e. quercetin, catachin and baicalein on hemin/nitrite/H2O2 induced brain homogenate oxidation and nitration were studied. The results showed that hemin/nitrite/H2O2 system could effectively induce brain homogenate protein oxidation and nitration. Quercetin, catachin and baicalein dose-dependently inhibited hemin/nitrite/H2O2 system-induced protein nitration in a dose-dependent manner, the inhibition of protein nitration was in the order of quercetin>catachin>baicalein. These compounds also inhibited hemin/H2O2 system-induced lipid peroxidation, the inhibition order was baicalein >quercetin>catachin. However, these flavonoids showed marginal effect on hemin/nitrite/H2O2 system caused protein oxidation and thiol oxidation. The inhibition activities of flavonoids on hemin/nitrite/H2O2 system-induced protein nitration may closely relate to their radical scavenging activities, since the inhibition order of protein nitration is the same as the radical scavenging order. These results indicate hemin/nitrite/H2O2 system induces different types of oxidative assault on bio-molecules. Flavonoids could act as antioxidants inhibiting ROS and RNS caused brain damage.

Abstract: Hemin–nitrite–H2O2 system may play a role in liver oxidative injury in some pathological events. In this paper, the effects of the three active components of the root of Scutellaria baicalensis Georgi, i.e. baicalin, baicalein and wogonin, on hemin–nitrite–H2O2 induced liver injury were studied in liver homogenate, liver microsome and human hepatoblastoma cell line HepG2 cells. It was found that hemin–nitrite–H2O2 could induce liver homogenate protein nitration, lipid peroxidation and liver microsome protein oxidation; it also caused a decrease of HepG2 cells viability. Baicalein, baicalin and wogonin could inhibit protein nitration and lipid peroxidation in liver homogenate as well as in HepG2 cells in a dose-dependent manner, the inhibition order was baicalein>baicalin≫wogonin. These three flavonoids also inhibited the oxidation of protein in liver microsome, the decrease of cell viability and the content of GSH in HepG2 cells, among which baicalin represented the most inhibitory effect. Besides, hemin–H2O2 induced cell injury could be augmented with the existence of nitrite, indicating protein nitration involved in hemin–nitrite–H2O2 induced liver injury. These results demonstrated hemin–nitrite–H2O2 could induce liver injury through oxidizing or nitrating different biomolecules. Baicalein, baicalin and wogonin could inhibit hemin–nitrite–H2O2 induced liver injury in dose-dependent manners by inhibiting oxidation and nitration. [Copyright &y& Elsevier]

Oxidative stress is associated with most traumatic or pathological bone defects, and seriously affects the effect of implantation. The construction of antioxidative and osteogenic coatings is of great significance to accelerate the bone regeneration of implants. In this study, baicalein (BAI), a nature flavonoid drug, was loaded in bovine serum albumin (BSA) by desolvent method to prepare BAI-BSA composite protein, and tannic acid (TA)/BAI-BSA coatings were further built via layer by layer self-assembly technology. BAI-BSA possesses good biocompatibility that showed no cytotoxicity to osteoblasts and erythrocytes, and helps to enhance the activity of alkaline phosphatase (ALP) and promote the formation of osteogenic mineralized calcium nodules. After assembled with TA, BAI-BSA coating significantly promoted cell adhesion and in vitro osteogenic mineralization of MC3T3-E1. Moreover, BAI drug loading improved the antioxidative function of BSA coatings effectively. The scavenging rates of (TA/BAI-BSA-10) 4 for ABTS+• and DPPH• free radicals were 69.6 ± 16.1 % and 53.4 ± 2.4 %, respectively. At cellular level, the TA/BAI-BSA coating effectively inhibited the impact of oxidative stress on the oxidative damage of osteoblasts. The drug-loaded protein coatings possess both great antioxidative and osteogenic functions, which have important potential in the field of bone repair. [ABSTRACT FROM AUTHOR]

Human islet amyloid polypeptide (hIAPP)-mediated cytotoxicity is identified as a potential target for developing new anti-diabetic molecules. Herein, we investigated the effect of the major bioactive compounds of Scutellaria baicalensis Georgi (S. baicalensis), including baicalein, baicalin, wogonin and oroxylin A, on hIAPP aggregation. We found that all of these compounds inhibited hIAPP fibril formation in a dose-dependent manner. But baicalein and baicalin, especially baicalein are more effective than wogonin and oroxylin A in stabilizing hIAPP monomers and eliminating toxic hIAPP assembly, suggesting that flavonoids with ortho-hydroxyl group on the A-ring exhibited higher anti-hIAPP nucleation potential than those without this structure. This stimulated our interest in further studying the possible structure-activity relationship between polyphenol and hIAPP aggregation inhibition. Our results demonstrated that flavonoids with ortho-hydroxyl group on the B-ring are also more effective against hIAPP nucleation than those without this structure. These results suggest that the ortho-hydroxybenzene structure is a key structural feature required for polyphenols to effectively inhibit hIAPP nucleation. This was further confirmed by the effects of polyphenol and phenols in inhibiting hIAPP nucleation. The conclusion that pyrogallol-type polyphenols are potential lead inhibitors may provide a valuable structural template for the further development of polyphenol-based inhibitor of amyloid peptides. [ABSTRACT FROM AUTHOR]

Abstract: Oxidative injury has been implicated in the pathogenesis of numerous neurodegenerative diseases. Recently, it has been found that with the existence of hydrogen peroxide and nitrite, hemin catalyzes protein nitration. We hypothesize under certain pathological conditions, hemin catalyzed protein nitration may happen in the brain. In this paper, the effects of three flavonoids, i.e. quercetin, catachin and baicalein on hemin/nitrite/H2O2 induced brain homogenate oxidation and nitration were studied. The results showed that hemin/nitrite/H2O2 system could effectively induce brain homogenate protein oxidation and nitration. Quercetin, catachin and baicalein dose-dependently inhibited hemin/nitrite/H2O2 system-induced protein nitration in a dose-dependent manner, the inhibition of protein nitration was in the order of quercetin>catachin>baicalein. These compounds also inhibited hemin/H2O2 system-induced lipid peroxidation, the inhibition order was baicalein >quercetin>catachin. However, these flavonoids showed marginal effect on hemin/nitrite/H2O2 system caused protein oxidation and thiol oxidation. The inhibition activities of flavonoids on hemin/nitrite/H2O2 system-induced protein nitration may closely relate to their radical scavenging activities, since the inhibition order of protein nitration is the same as the radical scavenging order. These results indicate hemin/nitrite/H2O2 system induces different types of oxidative assault on bio-molecules. Flavonoids could act as antioxidants inhibiting ROS and RNS caused brain damage. [Copyright &y& Elsevier]