Jihong Yao

Dalian Medical University, Lü-ta-shih, Liaoning, China

Are you Jihong Yao?

Claim your profile

Publications (17)32.09 Total impact

  • [Show abstract] [Hide abstract]
    ABSTRACT: High-mobility group box 1 (HMGB1) is essential in the response to injury during sepsis. We hypothesized that resveratrol (RESV) administration would inhibit nuclear-cytoplasmic HMGB1 translocation in hepatocytes, which is associated with sirtuin 1 (SIRT1) up-regulation. We investigated the regulatory role of SIRT1 in HMGB1 nucleocytoplasmic translocation and its effect on sepsis-induced liver injury.
    Shock (Augusta, Ga.) 07/2014; · 2.87 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Intestinal ischemia-reperfusion (I/R) is a serious clinical dilemma with high morbidity and mortality. Remote organ damage, especially acute lung injury and liver injury are common complications that contribute to the high mortality rate. We previously demonstrated that activation of PKCβII is specifically involved in the primary injury of intestinal I/R. Considering the tissue-specific features of PKC activation, we hypothesized that some kind of PKC isoform may play important roles in the progression of secondary injury in the remote organ. Mice were studied in in vivo model of intestinal I/R. The activation of PKC isoforms were screened in the lung and liver. Interestingly, we found that PKCβII was also activated exclusively in the lung and liver after intestinal I/R. PKCβII suppression by a specific inhibitor, LY333531, significantly attenuated I/R-induced histologic damage, inflammatory cell infiltration, oxidative stress, and apoptosis in these organs, and also alleviated systemic inflammation. In addition, LY333531 markedly restrained p66shc activation, mitochondrial translocation, and binding to cytochrome-c. These resulted in the decrease of cytochrome-c release and caspase-3 cleavage, and an increase in glutathione and glutathione peroxidase. These data indicated that activated PKC isoform in the remote organ, specifically PKCβII, is the same as that in the intestine after intestinal I/R. PKCβII suppression protects against remote organ injury, which may be partially attributed to the p66shc-cytochrome-c axis. Combined with our previous study, the development of a specific inhibitor for prophylaxis against intestinal I/R is promising, to prevent multiple organ injury.
    Apoptosis : an international journal on programmed cell death. 06/2014;
  • [Show abstract] [Hide abstract]
    ABSTRACT: Background This study investigated the role of Sirtuin 1 (SIRT1)/FOXO3 pathway, and a possible protective function for Icariin (ICA), in intestinal ischemia/reperfusion (I/R) injury and hypoxia/reoxygenation (H/R) injury. Materials and Methods Male Sprague-Dawley rats were pretreated with different doses of ICA (30 and 60 mg/kg) or olive oil as control 1 h before intestinal I/R. Caco-2 cells were pretreated with different concentrations of ICA (25, 50 and 100 μg/ml), then subjected to hypoxia/reoxygenation (H/R)-induced injury. Results The in vivo results demonstrated that ICA pretreatment significantly improved I/R-induced tissue damage and decreased serum tumor necrosis factor α and interleukin 6 levels. Changes of MnSOD, Bcl-2 and Bim were also reversed by ICA, and apoptosis was reduced. Importantly, the protective effects of ICA were positively associated with SIRT1 activation. Increased SIRT1 expression, as well as decreased acetylated FOXO3 expression, was observed in Caco-2 cells pretreated with ICA. Additionally, the protective effects of ICA were abrogated in the presence of SIRT1 inhibitor nicotinamide (NAM). This suggests that ICA exerts a protective effect upon H/R injury through activation of SIRT1/FOXO3 signaling pathway. Accordingly, the SIRT1 activator resveratrol achieved a similar protective effect as ICA upon H/R injury, whereas cellular damage resulting from H/R was exacerbated by SIRT1 knockdown and NAM. Conclusions SIRT1, activated by ICA, protects intestinal epithelial cells from I/R injury by inducing FOXO3 deacetylation both in vivo and in vitro These findings suggest that the SIRT1/FOXO3 pathway can be a target for therapeutic approaches intended to minimize injury resulting from intestinal dysfunction.
    Journal of Surgical Research 01/2014; · 2.02 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Intestinal ischemia-reperfusion (I/R) injury is a serious clinical pathophysiological process that may result in acute local intestine and remote liver injury. Protocatechuic acid (PCA), which has been widely studied as a polyphenolic compound, induces expression of antioxidative genes that combat oxidative stress and cell apoptosis. In this study, we investigated the effect of PCA pretreatment for protecting intestinal I/R-induced local intestine and remote liver injury in mice. Intestinal I/R was established by superior mesenteric artery occlusion for 45 min followed by reperfusion for 90 min. After the reperfusion period, PCA pretreatment markedly alleviated intestine and liver injury induced by intestinal I/R as indicated by histological alterations, decreases in serological damage parameters and nuclear factor-kappa B and phospho-foxo3a protein expression levels, and increases in glutathione, glutathione peroxidase, manganese superoxide dismutase protein expression, and Bcl-xL protein expression in the intestine and liver. These parameters were accompanied by PCA-induced adaptor protein p66shc suppression. These results suggest that PCA has a significant protective effect in the intestine and liver following injury induced by intestinal I/R. The protective effect of PCA may be attributed to the suppression of p66shc and the regulation of p66shc-related antioxidative and antiapoptotic factors.
    The Scientific World Journal 01/2014; 2014:387640. · 1.73 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Salvianolic acid B (SalB) is isolated from the traditional Chinese medical herb salvia miltiorrhiza. It has many biological and pharmaceutical activities. This study aimed to investigate the effect of SalB on acute ethanol-induced hepatic injury in rats and to explore the role of SIRT1 in this process. The results showed that pretreatment with SalB significantly reduced ethanol-induced elevation in aminotransferase activities, decreased hepatotoxic cytokine levels such as Interleukin-6 (IL-6), and increased the antioxidant enzyme activity. Moreover, SalB pretreatment reversed the increase in NF-κB, cleaved caspase-3 and decrease in B-cell lymphoma-extra large (Bcl-xL) caused by ethanol exposure. Importantly, SalB pretreatment significantly increased the expression of SIRT1, a NAD+-dependent deacetylase, whereas the increase in SIRT1 was accompanied by decreased acetyl-p53 expression. In HepG2 cells, SalB pretreatment increased SIRT1 expression in a time and dose-dependent manner and such an increase was abrogated by siRNA knockdown of SIRT1. Additionally, inhibition of SIRT1 significantly increased the acetylation of p53, and blocked SalB-induced acetylation of p53 down-regulation. Collectively, this study indicated that SalB can alleviate acute ethanol-induced hepatocyte apoptosis through SIRT1-mediated deacetylation of p53 pathway.
    Toxicology Letters 01/2014; · 3.15 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Objective. In this study, we investigated the protective effect and mechanism of curcumin on a rat model of intestinal ischemia/reperfusion (I/R), which induces an acute liver lesion. Methods. Curcumin was injected into rats in the curcumin groups through left femoral vein. The same volume of vehicle (0.9% normal saline) was injected into sham and I/R groups. Blood and liver tissue were gathered for serological and histopathological determination. Results. Intestinal I/R led to severe liver injury manifested as a significant increase in serum AST and ALT levels; all of those were reduced by treatment with curcumin. Simultaneously, the activity of SOD in liver decreased after intestinal I/R, which was increased by curcumin treatment. On the other hand, curcumin reduced MPO activity of liver tissue, as well as serum IL-6 and TNF-α levels observably. This is in parallel with the decreased level of liver intercellular cell adhesion molecule-1 (ICAM-1) and nuclear factor-κB (NF-κB) expression. Conclusion. Our findings suggest that curcumin treatment attenuates liver lesion induced by intestinal I/R, attributable to the antioxidative and anti-inflammatory effect via inhibition of the NF-κB pathway.
    Oxidative medicine and cellular longevity. 01/2014; 2014:191624.
  • [Show abstract] [Hide abstract]
    ABSTRACT: Activated macrophage infiltration into the lungs is paramount in the pathogenesis of acute lung injury (ALI) induced by intestinal ischemia-reperfusion (I/R). Omega-3 polyunsaturated fatty acid (ω-3 PUFA) is a potent activator of the Adenosine 5'-monophosphate-activated protein kinase-sirtuin1 (AMPK/SIRT1) pathway against macrophage inflammation. We aimed to evaluate whether ω-3 PUFAs may protect against ALI induced by intestinal I/R via the AMPK/SIRT1 pathway. Ischemia in male Wistar rats was induced by superior mesenteric artery occlusion for 60 min and reperfusion for 240 min. One milliliter per day of fish-oil emulsion (FO emulsion, containing major ingredients as ω-3 PUFAs) or normal saline (control) was administered by intraperitoneal injection for three consecutive days to each animal. All animals were sacrificed at the end of reperfusion. Blood and tissue samples were collected for analysis. Intestinal I/R caused intestinal and lung injury, evidenced by severe lung tissue edema and macrophage infiltration. Pretreatment with FO emulsion improved the integrity of microscopic structures in the intestine and lungs. Intestinal I/R induced the expression of macrophage-derived mediators (macrophage migration inhibitory factor and macrophage chemoattractant protein-1), inflammatory factors (nuclear factor κB, tumor necrosis factor α, interleukin 6, and interleukin 1β), and proapoptosis factor p66shc. There was a decrease in the expression of AMPK, SIRT1, and claudin 5. FO emulsion significantly inhibited macrophage infiltration into the lungs, inflammatory factor expression, and p66shc phosphorylation. Importantly, FO emulsion restored AMPK, SIRT1, and claudin 5 in the lungs. Pretreatment with ω-3 PUFAs effectively protects intestinal and lung injury induced by intestinal I/R, reduces macrophage infiltration, suppresses inflammation, inhibits lung apoptosis, and improves the lung endothelial barrier after intestinal I/R in a manner dependent on AMPK/SIRT1. Thus, there is a potential for developing AMPK/SIRT1 as a novel target for patients with intestinal I/R-induced ALI.
    Journal of Surgical Research 10/2013; · 2.02 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Salvianolic acid A (SalA) is a phenolic carboxylic acid derivative extracted from Salvia miltiorrhiza. It has many biological and pharmaceutical activities. The purpose of this study was to investigate the effect of SalA on concanavalin A (ConA)-induced acute hepatic injury in Kunming mice and to explore the role of SIRT1 in such an effect. The results showed that in vivo pretreatment with SalA significantly reduced ConA-induced elevation in serum alanine transaminase (ALT) and aspartate transaminase (AST) activities and decreased levels of the hepatotoxic cytokines such as interferon-gamma (IFN-γ) and tumor necrosis factor-alpha (TNF-α). Moreover, the SalA pretreatment ameliorated the increases in NF-κB and in cleaved caspase-3 caused by ConA exposure. Whereas, the pretreatment completely reversed expression of the B-cell lymphoma-extra large (Bcl-xL). More importantly, the SalA pretreatment significantly increased the expression of SIRT1, a NAD(+)-dependent deacetylase, which was known to attenuate acute hypoxia damage and metabolic liver diseases. In our study, the increase in SIRT1 was closely associated with down-regulation of the p66 isoform (p66shc) of growth factor adapter Shc at both protein and mRNA levels. In HepG2 cell culture, SalA pretreatment increased SIRT1 expression in a time and dose-dependent manner and such an increase was abrogated by siRNA knockdown of SIRT1. Additionally, inhibition of SIRT1 significantly reversed the decreased expression of p66shc, and attenuated SalA-induced p66shc down-regulation. Collectively, the present study indicated that SalA may be a potent activator of SIRT and that SalA can alleviate ConA-induced hepatitis through SIRT1-mediated repression of the p66shc pathway.
    Toxicology and Applied Pharmacology 08/2013; · 3.98 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: SCOPE: Flavonoids have well-known antioxidant, anti-inflammatory, and anti-cancer activities. Isoflavone genistein is considered a potent antioxidant agent against oxidative stress. Although several mechanisms have been proposed, a clear antioxidant mechanism of genistein is still remained to be answered. METHODS AND RESULTS: In this study, we focused on the concerted effects on expression of Nrf2 and phase II enzyme pathway components. Transient transfection assays, RT-PCR and immunoblot analysis were performed to study its molecular mechanisms of action. In Caco-2 cells, treatment with genistein markedly attenuated H(2) O(2) -induced peroxide formation; this amelioration was reversed by buthionine sulfoximine(GCLC inhibitor) and zinc protoporphyrin(HO-1 inhibitor). Genistein increased HO-1 and GCLC mRNA and protein expression. Genistein treatment activated the ERK1/2 and PKC signaling pathway; therefore increased Nrf2 mRNA and protein expression. The roles of the ERK1/2 and PKC signaling pathway were determined using PD98059 (ERK1/2 inhibitor) and GF109203X (PKC inhibitor) and RNA interference directed against Nrf2. Both inhibitors and siNrf2 abolished genistein-induced HO-1 and GCLC protein expression. These results suggest the involvement of ERK1/2, PKC, and Nrf2 in inducing HO-1 and GCLC by genistein. CONCLUSION: Our studies show that genistein up-regulated HO-1 and GCLC expression through the EKR1/2 and PKC /Nrf2 pathways during oxidative stress.
    Molecular Nutrition & Food Research 12/2012; · 4.31 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: High-speed counter-current chromatography (HSCCC) coupled with a reverse micelle solvent system was successfully developed to separate three proteins from Momordica charantia. Suitable HSCCC conditions were carefully optimized as follows: the stationary phase was a reverse micellar phase composed of isooctane and 50mM bis-(2-ethylhexyl)-1-sulfosuccinate sodium (AOT). The mobile phase contained mobile phase A (50mM Tris-HCl buffer containing 50mM KCl at pH 7.0) for forward-extraction and mobile phase B (50mM Tris-HCl buffer containing 0.5M KCl at pH 10.0) for back-extraction. The flow rate, detection wavelength and column temperature were set at 1.5 ml/min, 280 nm and 4 °C, respectively. Under these conditions, three fractions (I, II and III) were separated, which showed high purity when analyzed by sodium dodecyl sulfate polyacrylamide gel electrophoresis (SDS-PAGE). The structures of these proteins were then identified by MALDI-TOF/TOF-MS/MS and compared with the NCBInr database. Fractions I and III were identified as resistance-like protein P-B and pentatricopeptide repeat-containing protein, respectively, which were found in M. charantia for the first time. However, fraction II, which is thought to be a new protein, was not identified, and further investigations on this fraction are required. The anticancer activities of these three proteins on the human gastric cancer cell line SGC-7901 were evaluated in vitro. The results indicated that fraction II has excellent anticancer activity (IC(50)=0.116 mg/ml for 48 h treatment). This is the first report on the use of HSCCC to isolate proteins from M. charantia.
    Journal of chromatography. B, Analytical technologies in the biomedical and life sciences 03/2012; 895-896:77-82. · 2.78 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: The total flavonoids (TFs) from Rosa laevigata Michx fruit showed hepatoprotective and antioxidant activities. However, the safety of this natural product has not been investigated. In the present paper, a 90-day subchronic toxicity study was conducted, and the tested TFs was orally administered to rats at the doses of 500, 1000 and 2000mg/kg/day. The toxicity of the TFs was evaluated on base of ophthalmic examination, body weight, feed/water consumption, urinalysis, hematology, clinical biochemistry and pathology. No toxic signs of the TFs at the doses of 500 and 1000mg/kg/day were observed. However, decreased PLT was found in the 2000mg/kg/day groups and increased intercellular space of myocardial cells was observed in the male 2000mg/kg/day group compared with control. A significant increase in the relative cardiac weight was observed in the male 1000 and 2000mg/kg/day groups. And the significant decrease in the absolute and relative weight of adrenals in the female 1000 and 2000mg/kg groups was happened. The TFs could cause mild side effects at the dose of 1000mg/kg/day in males and females. Thus, the dose of 500mg/kg/day for male and female were selected as the no-observed-adverse-effect level (NOAEL). The present study provides useful data for subsequent researches and new drug exploration of the TFs from R. laevigata Michx fruit.
    Regulatory Toxicology and Pharmacology 03/2012; 62(2):221-30. · 2.13 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: A successful method of preparative high-speed counter-current chromatography (HSCCC) was established for direct isolation and purification of hydrolysis products of Epimedium koreanum Nakai to obtain the secondary glycosides and aglycons of flavonoids in E. koreanum. The two-phase solvent systems of HSCCC composed n-hexane-ethyl acetate-methanol-water at the ratios of 6:3.5:6:5 (v/v) and 6:3.5:8:5 (v/v) were used in a stepwise elution. Totally, 60.1 mg of Fraction I that would be isolated and purified by preparative HPLC, 9.4 mg of icartin (4), 3.5 mg of desmethylicartin (5), 4.7 mg of 3ethyoxyl-icartin (6), 7.3 mg of anhydroicaritin (7) and 10.1 mg of β-anhydroicaritin (8) were obtained in one-step separation from 100 mg of the crude materials with purities of 97.7%, 96.2%, 99.2%, 99.5% and 91.0%, respectively. And Fraction I of HSCCC was purified by the preparative HPLC to obtain 12.7 mg of pletypetaloside (I-1), 6.8 mg of icariside I (I-2) and 16.3 mg of 3ethyoxyl-pletypetaloside (I-3) with purities of 90.8%, 93.4% and 99.2%. All of the chemical structures were identified on the basis of widely spectral technology including 2D-NMR. Among them, compounds I-3 and6 are novel.
    Journal of Liquid Chromatography &amp Related Technologies 01/2012; · 0.57 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: MG132 is a potent antioxidant and has been reported to play a protective role in ischemia/reperfusion (I/R) of many organs. Recent studies have shown that the Aryl hydrocarbon receptor (AhR) may play a beneficial role in I/R of many organs and an AhR agonist has been implicated in an anti-inflammatory role. MG132 might function as an AhR agonist through proteasome inhibition, possibly through the inhibition of NFκB. Herein, we hypothesized that MG132 may play a protective role in liver injury induced by intestinal I/R and we analyzed the expression behavior of AhR and NFκB to determine whether the two factors play a role in intestinal I/R. Thirty-two Sprague-Dawley rats were divided into four groups: control, I/R, MG132 control, and MG132 pretreatment. The I/R and MG132 pretreatment groups were subjected to mesenteric arterial ischemia for 1 h and reperfusion for 3 h. The control and MG132 control groups underwent surgical preparation including isolation of the superior mesenteric artery (SMA) without occlusion. The MG132 control and MG132 pretreatment groups were subjected to intraperitoneal administration of 0.5 mg/kg MG132 30 min before surgery. We collected serum specimens to measure TNF-α, IL-6, liver tissue levels of malondialdehyde (MDA), AhR, and cyp1a2; NFκB, IκBα, and ICAM-1 were also tested. Histologic changes of liver and intestine were subsequently evaluated. Compared with the control group, significant increases in MDA, NFκB, and ICAM-1 levels were accompanied by decreases in AhR, cyp1a2, and IκBα expression in the liver in the I/R group, which is consistent with liver and intestinal tissue injury. MG132 blocked the alterations of the indicators above. There were no changes in the MG132 control group compared with the control group in the indicators above. This study demonstrated that MG132 has a significant effect in protection against liver injury induced by intestinal I/R, which may be due to modulation of the AhR and NFκB pathways.
    Journal of Surgical Research 09/2011; 176(1):63-73. · 2.02 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Carboxymethyl cellulose sodium (CMC) was used as the template to prepare zirconium hydroxide nanoparticles. The resulted Zr-CMC was composed of about 29.4wt% CMC and amorphous zirconium hydroxide. Zirconium hydroxide nanoparticles in size of 20–50nm were encapsulated by CMC, which could improve the stability of zirconium hydroxide in water. Trichosanthes kirilowii (TK) is a traditional Chinese medicine, which is rich in starch. TK starch is attempted to be plasticized with glycerol to obtain glycerol-plasticized starch (GPS) in the casting process. And Zr-CMC as the filler was loaded in GPS matrix. Since Zr-CMC could form the good interaction with GPS matrix, Zr-CMC filler could be dispersed well in GPS matrix; thereby, improve the mechanical properties and water barrier of GPS matrix.
    Carbohydrate Polymers - CARBOHYD POLYM. 01/2011; 86(4):1699-1704.
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: The effect of Laennec, a hydrolyte of human placenta, on immune-mediated liver injury was investigated in vivo and in vitro in murine. Vena caudalis administration of concanavalin A (Con A) was employed to establish an in vivo liver-injury model, and in vitro hepatotoxicity was induced by 8 h interaction between Con A pre-treated hepatocytes and Con A-stimulated autologous splenic lymphocytes. Laennec was used for pre-treatment in the two models. Laennec decreased biochemical marker activity (alanine aminotransferase, ALT; lactate dehydrogenase, LDH) in serum and recovered the activity of superoxide dismutase (SOD) and myeloperoxidase (MPO), as well as the content of malondialdehyde (MDA) and nitric oxide (NO) in liver tissue. We also found that the DNA ladder induced by Con A in vivo was attenuated by Laennec. Furthermore, the leakage of aspartate aminotransferase (AST) and LDH in the supernatant of the co-culture system was decreased by addition of Laennec. Potential protective mechanisms were elucidated by DNA fragmentation assay and intercellular adhesion molecule-1 (ICAM-1) induction/inhibition experiments. Results showed that ICAM-1, which is related to the interaction between hepatocytes and lymphocytes, was inhibited by Laennec. These findings indicated that Laennec has potent activity against immune-mediated liver injury.
    Biological & Pharmaceutical Bulletin 12/2008; 31(11):2040-4. · 1.85 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Fully soluble hemostatic fiber (FHF) is made from cotton yarn through a series of chemical reactions with NaOH and chloroacetic acid. The major component of FHF is carboxymethylcellulose. FHF is a kind of biodegradation macromolecule material that can disassociate into a low-molecular-weight compound or a simple substance by hydrolytic and enzymatic courses. The purpose of the present study is to investigate the hemostatic mechanism of FHF. The study indicated that FHF can stop bleeding by physical, chemical and physiological routes. In the physical route, expansion of carboxymethylcellulose in FHF stops bleeding by forming a mechanical clog after contacting with the blood. In the chemical route, the platelets can quickly aggregate around FHF and stimulate releasing and disaggregating reactions, after contacting with the rough surface of FHF, producing thrombus and hemostasis. In the physiological route, gluey particles with negative charges can activate intrinsic coagulation systems by activating the blood coagulation factor XII after FHF dissolution.
    Blood Coagulation and Fibrinolysis 10/2007; 18(6):555-8. · 1.25 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: A rapid, sensitive and specific method for the simultaneous quantification of resibufogenin (RBG) and 3-epi-resibufogenin (3-ERBG) in rat plasma was developed by using a liquid–liquid extraction procedure and liquid chromatography–electrospray ionization/tandem mass spectrometric (LC–ESI–MS/MS) analysis. The separation was performed by HPLC on a reversed phase C18 HPLC column (150 × 2.1 mm, 3.5 μm) using a mobile phase of acetonitrilel-0.1% formic acid aqueous solution (45:55, v/v). The determination was performed by a triple-quadrupole mass spectrometer in the multiple reaction monitoring using positive mode of electrospray ionization (ESI). The calibration curves were both linear (R > 0.995) over the concentration range of 3.0–5,000 ng mL−1, and the lower limits of quantification were 3.0 ng mL−1 for both RBG and 3-ERBG. The intra-day and inter-day precisions (% RSD) were all less than 15%, and the accuracies (%RE) were within the range of ±15%. The mean recoveries of RBG, 3-ERBG and IS were over 82.7, 84.8 and 90.0% (n = 6), respectively. The method was proved to be rapid, sensitive and specific, and has been successfully applied to determine RBG and its major metabolite 3-ERBG in rat plasma after oral administration of RBG for pharmacokinetic study. Comparison of pharmacokinetic data with anti-tumor activities of RBG and ERBG suggested that 3-ERBG, as a major metabolite of RBG in rats, was perhaps also a bioactive form of RBG in vivo.
    Chromatographia 75(3-4). · 1.44 Impact Factor