Sodium Tanshinone IIA Sulfonate Research Articles

Sodium Tanshinone IIA Sulfonate Ameliorates Bladder Fibrosis in a Rat Model of Partial Bladder Outlet Obstruction by Inhibiting the TGF-β/Smad Pathway Activation.

Transforming growth factor (TGF)-β1 is known to play a pivotal role in a diverse range of biological systems including modulation of fibrosis in several organs. The precise role of TGF-β/Smad signaling in the progression of bladder fibrosis secondary to partial bladder outlet obstruction (PBOO) is yet to be conclusively. Using a rat PBOO model, we investigated TGF-β1 expression and exaimined whether sodium tanshinone IIA sulfonate (STS) could inhibit TGF-β/Smad signaling pathway activation and ameliorate bladder fibrosis. Forty-eight female Sprague-Dawley rats were randomly divided into three groups: sham operation group (n = 16), PBOO operation without STS treatment group (n = 16) and PBOO operation with STS treatment group (n = 16). Thirty-two rats underwent the operative procedure to create PBOO and subsequently received intraperitoneal injections of STS (10 mg/kg/d; n = 16) or vehicle (n = 16) two days after the surgery. Sham surgery was conducted on 16 rats, which received intraperitoneal vehicle injection two days later. In each of the three groups, an equal number of rats were sacrificed at weeks 4 and 8 after the PBOO or sham operation. The TGF-β/Smad signaling pathway was analyzed using western blotting, immunohistochemical staining and reverse transcriptase polymerase chain reaction (RT-PCR). One-way analysis of variance was conducted to draw statistical inferences. At 4 and 8 weeks, the expression of TGF-β1 and phosphorylated Smad2 and Smad3 in STS-treated PBOO rats was significantly lower than in the PBOO rats not treated with STS. Alpha smooth muscle actin (α-SMA), collagen I and collagen III expression at 4 and 8 weeks post PBOO was lower in STS-treated PBOO rats when compared to that in PBOO rats not treated with STS. Our findings indicate that STS ameliorates bladder fibrosis by inhibiting TGF-β/Smad signaling pathway activation, and may prove to be a potential therapeutic measure for preventing bladder fibrosis secondary to PBOO operation.

Sodium tanshinone IIA sulfonate ameliorates ischemia-induced myocardial inflammation and lipid accumulation in Beagle dogs through NLRP3 inflammasome

BackgroundThe activation of NOD-like receptor (NLR) family, pyrin-domain containing 3 (NLRP3) inflammasome has now been proven to have a close connection with myocardial ischemia (MI) during acute phase, but the mechanisms are not completely clear. This study investigated the role of NLRP3 inflammasome in pathogenesis of MI injury including inflammation and lipid accumulation, as well as the effects of sodium tanshinone IIA sulfonate (STS) and diltiazem hydrochloride (DI). MethodsOcclusion of left anterior descending (LAD) in canines was employed to induce MI. STS and DI were given intravenously 15min after LAD occlusion. Cardiac function, inflammation and lipid levels, as well as related signaling pathways were determined. ResultsMI induced in Beagle dog was characterized by elevated ST-segment and increased CK-MB level in serum. Cardiac NLRP3 inflammasome was activated with elevated myocardial IL-1β and IL-18 concentrations mediated by ROS over-production and TXNIP over-expression in MI dogs. Additionally, pro-inflammatory cytokines induced impairment of cardiac JAK2-STAT3 inflammatory pathway and insulin signaling pathway in this model, resulting in down-regulation of cardiac PPAR-α expression, subsequently causing lipid metabolism disorders characterized by elevation of myocardial lipid concentrations. These abnormalities were attenuated by the treatment of STS and DI. ConclusionsThese data firstly demonstrated that cardiac NLRP3 inflammasome activation driven by cardiac ROS over-production and TXNIP up-expression resulted in impairment of the JAK2–STAT3 and insulin signaling pathways, leading to disorder of lipid metabolism in myocardial ischemic dogs through PPAR-α over-expression. STS and DI might target cardiac NLRP3 inflammasome in preventing MI injury.

Sodium tanshinone IIA sulfonate inhibits cigarette smoke-induced airway inflammation via regulating cystic fibrosis transmembrane conductance regulator-mediated pathway (HUM1P.263)

Abstract Cystic fribrosis transmembrane conductance regulator (CFTR) is an important anti-inflammatory protein and confers to development of chronic obstructive pulmonary disease (COPD). Sodium tanshinone IIA sulfonate (STS) has been reported to be anti-inflammatory under various stimuli exposure, however, the underlying mechanisms were not fully understood. In this study, we found exposure to cigarette smoke (CS) led to COPD in mice, manifested by reduction in lung function, increases of inflammatory cell counts in bronchial alveolar lavage fluid , and alveoli enlargement; these changes were associated with reduced expression and chloride current of CFTR, greater activation of ERK1/2 and Nrf2, and greater levels of IL-6 and IL-8 in the lung. Treatment of STS aerosol (10mg·kg-1·day-1) attenuated these responses in COPD mice. In 16HBE human bronchial epithelial cells, exposure to CS extract resulted in reduced CFTR expression, activation of ERK1/2 and Nrf2, and increased IL-6 and IL-8 release; these were potentiated by rise of intracellular concentration of Cl- (70 mM), pretreatment with CFTR inhibitor inh-172 (10 mM) or Nrf2 activation, yet prevented by knockdown of Nrf2, inhibition of ERK1/2 activation, or STS (25uM) treatment. These results indicate that STS could inhibit CS-induced COPD development by preventing CS-induced CFTR reduction, thus inhibiting Cl--ERK1/2-Nrf2 mediated pro-inflammatory cytokine production in airway epithelial cells.

Sodium tanshinone IIA sulfonate attenuates the transforming growth factor-β1-induced differentiation of atrial fibroblasts into myofibroblasts in vitro.

The differentiation of atrial fibroblasts into myofibroblasts is a critical event in atrial fibrosis. One of the most important factors in atrial fibroblast differentiation is transforming growth factor-β1 (TGF-β1). Accumulating evidence indicates that sodium tanshinone IIA sulfonate (STS) possesses antifibrotic properties. In this study, we therefore investigated whether STS attenuates the TGF-β1‑induced differentiation of atrial fibroblasts. TGF-β1 enhanced collagen production, collagen synthesis and the expression of collagen type I and III, as shown by hydroxyproline assay, collagen synthesis assay and western blot analysis, respectively. In addition, as shown by immunohistochemistry and western blot analysis, TGF-β1 enhanced the expression of α-smooth muscle actin (α-SMA), which is the hallmark of myofibroblast differentiation. These responses were attenuated by treatment with STS. In addition, STS suppressed the TGF-β1‑induced expression of phosphorylated (p)Smad/pSmad3 expression and nuclear translocation. Furthermore, STS suppressed extracellular signal-regulated kinase (ERK) phosphorylation. In conclusion, the current study demonstrates that STS exerts antifibrotic effects by modulating atrial fibroblast differentiation through ERK phosphorylation and the Smad pathway.

Sodium tanshinone IIA sulfonate for reduction of periprocedural myocardial injury during percutaneous coronary intervention (STAMP trial): Rationale and design

a Second Clinical Medical College, Guangzhou University of Chinese Medicine, Guangzhou 510405, China b Department of Critical Care Medicine, Guangdong Provincial Hospital of Chinese Medicine, Guangzhou 510120, China c Chinese Medicine Research Institute, Tianjin University of Chinese Medicine, Tianjin 300193, China d Physiology & Experimental Medicine, Hospital for Sick Children, Toronto M5G 0A4, Canada

Determination of Sodium Tanshinone Iia Sulfonate in Rat Plasma by High Performance Liquid Chromatography and its Application to Pharmacokinetics Studies

A rapid high performance liquid chromatography (HPLC) method for the determination of sodium tanshinone IIA sulfonate (STS) in rat plasma is developed and validated. Sample preparation is accomplished through protein precipitation with methanol. The analyte and internal standard tanshinone I sulfonate are separated on an Agilent Extend C18 analytical column, using a mixture of methanol and triethylamine (0.1) (60:40, v/v) as the mobile phase. The low limit of quantification is 0.2 μg/mL, and the method is linear over the concentration range of 0.2-50 μg/mL for STS. The within- and between-run precisions (RSD) are within 5.8, mean extraction yields are always higher than 93.40, and it proves to be stable during all sample storing, preparation and analytic procedures. The method is successfully applied to a pharmacokinetic study after an intravenous administration of STS to rats at a dose of 6 mg/ kg and pharmacokinetics is described by a three-compartment open model.

Effect of sodium tanshinone IIA sulfonate treatment in a rat model of preeclampsia.

Preeclampsia is a disorder of pregnancy with a significant impact on maternal and fetal health. The complexity of this multifactorial condition has precluded development of effective therapies and, although many potential pathways have been investigated, the etiology still requires clarification. Our group has investigated the scavenger lectin-like oxidized LDL (LOX-1) receptor, which may respond to factors released from the distressed placenta that contribute to the vascular pathologies observed in preeclampsia. Given the known beneficial effects of sodium tanshinone IIA sulfonate (STS; a component of Salvia miltiorrhiza) on vasodilation, reduction of oxidative stress, and lipid profiles, we have investigated its role as a potential treatment strategy. We hypothesized that STS would improve vascular endothelial function and, combined with a reduction in oxidative stress, would improve pregnancy outcomes in a rat model of preeclampsia (reduced uteroplacental perfusion pressure, RUPP). We further hypothesized this may occur via the action of STS on the LOX-1 and/or platelet-activating factor (PAF) receptor axes. The RUPP model increased maternal blood pressure, vascular oxidative stress, and involvement of the vascular PAF receptor. Treatment with STS during pregnancy decreased both oxidative stress and involvement of the PAF receptor; however, it also increased involvement of the LOX-1 receptor, which is in line with the concept that scavenger receptors, such as LOX-1 and PAF, are upregulated in response to ligand binding and/or under pathological conditions. In this model of preeclampsia, however, the vascular actions of STS did not lead to improvements in pregnancy outcome such as fetal biometrics or maternal blood pressure.

GW25-e3173 Inhibition of TRPC channels by the cardioprotective drug sodium tanshinone IIA sulfonate

Sodium tanshinone IIA sulfonate (STS) is a water-soluble derivative of tanshinone IIA, the major lipophilic component extracted from the root of Danshen ( Salvia Miltiorrhiza ). STS is clinically used in the treatment of myocardial infarction, coronary artery disease and other cardiovascular

Sodium tanshinone IIA sulfonate attenuates radiation-induced fibrosis damage in cardiac fibroblasts

The main pathological change in radiation-induced heart disease is fibrosis. Emerging evidence has indicated that sodium tanshinone IIA sulfonate (STS) was used for treating fibrosis diseases. The present study was undertaken to characterize the effect of STS on radiation-induced cardiac fibrosis (RICF) on cultured cardiac fibroblasts (CFs). CFs were irradiated with 1 or 2 Gy X-rays, and the expression of TGF-β1 and collagen I (Col-1) increased, indicating that low-dose X-rays promoted fibrosis damage effect. The fibrosis damage was accompanied by morphologic changes in the endoplasmic reticulum (ER), as well as an increase in the expression of the ER stress-related molecules, GRP78 and CHOP. Administration of STS reduced ROS production and decreased the expression of Col-1, TGF-β1, p-Smad2/3, GRP78, and CHOP in irradiated CFs, thus weakening the radiation-induced fibrosis damage and ER stress. Radiation-induced fibrosis damage was observed on a cellular level. The involvement of ER stress in radiation-induced fibrosis damage was demonstrated for the first time. STS attenuated the fibrosis damage effect in CFs and this effect may be related to its antioxidant action, and also related to its inhibition of ER stress and TGF-β1-Smad pathway. These results suggest that STS shows a good prospect in clinical prevention and treatment of RICF.

Sodium tanshinone IIA sulfonate and sodium danshensu open the placental barrier through down-regulation of placental P-glycoprotein in mice: Implications in the transplacental digoxin treatment for fetal heart failure

Sodium tanshinone IIA sulfonate and sodium danshensu open the placental barrier through down-regulation of placental P-glycoprotein in mice: Implications in the transplacental digoxin treatment for fetal heart failure

The cardioprotective effect of sodium tanshinone IIA sulfonate and the optimizing of therapeutic time window in myocardial ischemia/reperfusion injury in rats

ObjectiveThe protective effect of sodium tanshinone IIA sulfonate (STS) pretreatment against experimental myocardial ischemia/reperfusion (I/R) has been demonstrated previously, however its therapeutic effects and mechanism of action still remain unclear. The objective of this study was to investigate the therapeutic time window and potential mechanism of STS action on myocardial I/R injury in a rat model of myocardial I/R. MethodsRats received 30 min ischemia by complete ligation of the left ascending coronary artery, and then were reperfused for 24 h. STS (8 mg/kg) was administered intravenously 15 min before and at 0, 0.5, 1, 2, 4, 6 h after reperfusion. The infarct size and several consequences of myocardial I/R including myocardial zymogram, antioxidant status, cardiac function and microstructure disorder were evaluated 24 h after reperfusion. Furthermore, the effect of STS on heme oxygenase-1 (HO-1) protein expression and nuclear factor-κB (NF-κB) activation were also evaluated. ResultsIn the present study, the time point of optimal cardioprotective effect of STS was within 2 h after reperfusion, with declining effect at 4 h and no effect at 6 h after the onset of reperfusion. In addition, STS-mediated cytoprotection against oxidative stress and inflammatory responses was correlated with an increased HO-1 activity.. ConclusionsSTS could ameliorate cardiac dysfunction and variation of myocardial zymogram, up-regulate antioxidant systems. Moreover, modulation of HO-1 was involved in STS induced cardioprotection..

Tanshinone IIA sulfonate upregulated pulmonary artery smooth muscle peroxisome proliferator-activated receptor γ expression in monocrotaline induced pulmonary hypertension rat

To investigate the effect of sodium tanshinone IIA sulfonate (STS) on rat right ventricular systolic pressure (RVSP), mean right ventricular pressure (MRVP), right ventricular hypertrophy index [RV/(LV+S)], pulmonary vascular remodeling, and PPARγ protein expression in pulmonary artery smooth muscle of monocrotaline (MCT) induced rat pulmonary hypertension model. The pulmonary hypertension model was established by subcutaneously injection of MCT, and the rats were treated with or without STS for 21 days. After that, RVSP, mRVP and RV/(LV+S) were measured. Lung histopathological sections were prepared, and the lumen area, the wall thickness and arterial radius of pulmonary arteries were quantified using the Image Pro Plus 6.0 software. PPARγ protein expression in rat pulmonary artery smooth muscle was detected by Western blot. Compared with control group, the RVSP, mRVP were significantly increased in MCT group (P < 0.05), while in the MCT+STS group, it was decreased from (81.2 ± 1.9) and (28.6 ± 2.0) mmHg to (35.4 ± 8.3) and (14.1 ± 5.4) mmHg, respectively (P < 0.05). The RV/(LV+S) of MCT group was (0.57 ± 0.04), markedly higher than those of control group and control+STS group (0.33 ± 0.02) and (0.34 ± 0.02) , respectively, P < 0.05, while in MCT+STS group, the RV/(LV+S) was (0.43 ± 0.02), lower than that of MCT group (P < 0.05) ;The luminal area/total area of MCT group decreased to (27 ± 6)%compared with control rats (56.00 ± 3.00) % (P < 0.05) . The wall thickness/artery radius (WT%) of MCT group increased from (20 ± 4) % (control group) to (40 ± 3) % (P < 0.05) .In MCT+STS treated rats, luminal area/ total area and WT% were (39.0 ± 2.0) %and (31.0 ± 2.0) %, both statistically different from MCT group (P < 0.05) . The level of PPARγ protein in pulmonary artery smooth muscle of MCT group was (48 ± 4) %, lower than control group (100 ± 0) % (P < 0.05) .In the MCT+STS group, PPARγ protein expression was recovered (102 ± 3) %, (P < 0.05) . STS markedly decreased RVSP,MRVP, RV/(LV+S) and pulmonary vascular remodeling in MCT induced pulmonary hypertension rat, and PPARγ might be targeted as a key molecule during STS treatment.

Effect of sodium tanshinone ⅡA sulfonate on AngⅡ-induced atrial fibroblast collagen synthesis and TGF-β1 activation

Effect of sodium tanshinone ⅡA sulfonate on AngⅡ-induced atrial fibroblast collagen synthesis and TGF-β1 activation

Screening compounds of Chinese medicinal herbs anti-Marek's disease virus

Context: Marek’s disease (MD) seriously threatens the world poultry industry and has resulted in great economic losses. Chinese medicinal herbs are a rich source for lead compounds and drug candidates for antiviral treatments.Objective: To investigate the anti-MDV activity and mechanism of 20 compounds extracted from Chinese medicinal herbs.Materials and methods: Antiviral assay, time of addition experiments, and virucidal assay were performed on chicken embryo fibroblast cells. The 50% cytotoxic concentration and 50% effective concentration were determined and, accordingly, selectivity index and inhibition ratio were calculated.Results: Antiviral assay showed dipotassium glycyrrhizinate (DG) and sodium tanshinone IIA sulfonate (STS) exhibited significantly inhibitory activity against MDV in a dose-dependent manner. EC50 of DG and STS were 893.5 ± 36.99 µg/mL and 54.82 ± 2.99 µg/mL, and selective index (SI) were >3.36 and >9.12, respectively. Time of addition experiment and virucidal assay demonstrated DG inhibited viral replication in the full replication cycle and inactivated MDV particles in non-time-dependent manner, but STS interfered with the early stage of MDV replication and inactivated MDV particles in a time-dependent manner. Moreover, both DG and STS promoted apoptosis of cells infected by MDV.Discussion and conclusion: DG and STS have great potential for developing new anti-MDV drugs for clinic application.

Sodium Tanshinone Iia Sulfonate Inhibits Porcine Reproductive and Respiratory Syndrome Virus via Suppressing N Gene Expression and Blocking Virus-Induced Apoptosis

Porcine reproductive and respiratory syndrome virus (PRRSV) causes significant economic loss in the swine industry. Currently, there is no effective way to prevent PRRSV infection. Sodium tanshinone IIA sulfonate (STS), a natural compound derived from Salvia miltiorrhiza, was shown to possess anti-PRRSV activity, but the underlying mechanisms remain unclear. The objective of this study was to investigate the effect of STS on PRRSV-induced cell apoptosis and PRRSV N protein expression pattern. Relative quantification real-time PCR was used to evaluate the inhibition of STS on N gene expression. Simultaneously indirect immunofluorescence assay (IFA) and western blot were used to assess the effect on N protein expression. Apoptosis was analysed using fluorescence microscope with an annexin V-EGFP kit. The effect of STS on caspase-3 cleaving was assessed by western blot. Our results showed that STS could inhibit viral N gene expression at both the messenger RNA stage and at the protein level in PRRSV-infected cells in a dose-dependent manner. In addition, STS could also rescue PRRSV-induced apoptosis. Our data suggest that STS may serve as a base compound for developing more effective drugs against PRRSV infection.

Sodium Tanshinone IIA Sulfonate Inhibits the MEQ, Ul49 and VP22 Expression of Marek's Disease Virus

Our previous studies have demonstrated that sodium tanshinone IIA sulfonate (STS), a natural compound derived from Salviae Miltiorrhizae Radix et Rhizoma (Danshen), could effectively inhibit Marek's disease virus (MDV) infection both in vitro and in vivo, but the underlying mechanisms remain unclear. The main objective of the study was to explore the effect of STS on the meq, ul49 and VP22 expression of MDV in vitro. Quantitative real-time PCR (qRT-PCR) was used to analyse the effect of STS on meq and ul49 expression at both the DNA and messenger RNA (mRNA) level, and the effect of STS on VP22 was assessed by immunofluorescence assay and western blotting. The DNA and mRNA copy numbers of meq and ul49 significantly decreased in the groups treated with STS compared with MDV control (P<0.05), which indicated that STS could inhibit the expression of meq and ul49 at both the DNA and mRNA level. Moreover, the expression of VP22 encoded by ul49 was also significantly inhibited (P<0.05). STS possessed anti-MDV activity in chicken embryo fibroblasts. Its antiviral mechanisms may be ascribed to inactivating MDV directly, disturbing meq and ul49 replication and inhibiting the expression of VP22 encoded by ul49. These results suggested that STS is a promising natural compound to be further developed as an antiviral agent against MDV infection.

Sodium tanshinone IIA sulfonate protects rat myocardium against ischemia-reperfusion injury via activation of PI3K/Akt/FOXO3A/Bim pathway

To investigate the mechanisms underlying the protective effects of sodium tanshinone IIA sulfonate (STS) in an ischemia-reperfusion (I/R)-induced rat myocardial injury model. Male SD rats were iv injected with STS, STS+LY294002 or saline (NS) for 15 d. Then the hearts were subjected to 30 min of global ischemia followed by 2 h of reperfusion. Cardiac function, infarction size and area at risk were assessed. Cell apoptosis was evaluated with TUNEL staining, DNA laddering and measuring caspase-3 activity. In addition, isolated cardiomyocytes of neonatal rats were pretreated with the above drugs, then exposed to H2O2 (200 mol/L) for 1 h. Cell apoptosis was detected using flow cytometric assay. The levels of p-Akt, p-FOXO3A and Bim were examined with immunoblotting. Compared to NS group, administration of STS (20 mg/kg) significantly reduced myocardial infarct size (40.28%±5.36% in STS group vs 59.52%±7.28% in NS group), and improved the myocardial function as demonstrated by the increased values of dp/dtmax, LVDP and coronary flow at different reperfusion time stages. Furthermore, STS significantly decreased the rate of apoptotic cells (15.11%±3.71% in STS group vs 38.21%±7.83% in NS group), and reduced caspase-3 activity to nearly a quarter of that in NS group. Moreover, STS significantly increased the phosphorylation of Akt and its downstream target FOXO3A, and decreased the expression of pro-apoptotic gene Bim. Co-treatment with the PI3K inhibitor LY294002 (40 mg/kg) partially countered the protective effects induced by STS treatment. In isolated cardiomyocytes, STS exerted similar protective effects as shown in the ex vivo I/R model. STS pretreatment reduces infarct size and improves cardiac function in an I/R-induced rat myocardial injury model via activation of Akt/FOXO3A/Bim-mediated signal pathway.

Preparation, Characterization Evaluation of Tanshinone IIA Lipid Microspere and Comparative Study of Pharmacokinetics with Sodium Tanshinone IIA Sulfonate Injection

In this study, Tanshinone IIA lipid microspere (Tan-IIA-LM) was successfully prepared by an ultrasonic and high-pressure homogenization method. The particle size, zeta potential, drug entrapment efficiency and morphological properties of Tan-IIA-LM were characterized in detail. A pharmacokinetic comparative study of Tan-IIA-LM with Sodium Tanshinone IIA Silate (STS) injection was developed. A sensitive and specific HPLC method was established to determine the mass concentration of Tan-IIA and STS in rats plasma samples which were compared between Tan-IIA-LM and STS injection after single dose intravenous administration of 18.35μmol/kg and the results were fitted and analyzed by dedicated software. After intravenous administration, the AUC0-and Cmaxvalues of Tan-IIA were 2.14, 2.22 fold higher than STS. The clearance, apparent volume of distribution and mean residence time (MRT) of Tan-IIA were lower (P&lt;0.01) than STS; other pharmacokinetic parameters had no significant deviation (P&gt;0.05). The pharmacokinetic of Tan-IIA, STS have significant differences at the same molar doses and the AUC and Cmaxvalues of Tan-IIA were higher compared with STS.

Nanovesicles System for Rapid-Onset Sublingual Delivery Containing Sodium Tanshinone IIA Sulfonate: In vitro and In Vivo Evaluation

A novel formulation based on nanovesicles system for rapid-onset sublingual delivery of hydrophilic drug (sodium tanshinone IIA sulfonate, STS) was investigated. The nanovesicles system was composed of 1.5% soybean lecithin, 6% propylene glycol, and penetration enhancers (1% sodium dodecyl sulfate and 0.03% hyaluronan acid). The STS-loaded nanovesicles with an average diameter of 133 ± 9.04 nm and high entrapment efficiency of 85.65 ± 3.89% were characterized. The effects of permeation enhancers on the penetration of STS formulations were investigated using Franz diffusion cells in vitro, showing 86.1-235.8 times higher permeation rate than that of normal STS solution. The rapid symptom relief effect of the nanovesicles system on acute myocardial infarction rabbits was evaluated by in vivo study, ST-segment deviation(S and T wave abnormality in electrocardiogram) was attenuated markedly and rapidly within 5 min, infarct size of heart was significantly reduced and the biochemical indicators were substantially decreased, compared with the control groups (p < 0.05). This study provided a promising tool for the future sublingual delivery of hydrophilic compounds with the noninvasive and rapid onset clinical effect.

Effects of sodium tanshinone IIA sulfonate against Marek's disease virus in experimentally infected chickens

Chickens experimentally infected with Marek's disease virus J-1 strain were used to evaluate the anti-Marek's disease virus (MDV) activity of sodium tanshinone IIA sulfonate (STS) in vivo. Chickens in same group were kept in one pen and control group chickens were housed in negative pressure isolator. Chickens were treated with different dose of STS or ABOB for 21 consecutive days. Peripheral T lymphocyte proliferation, expression level of IFN-γ and IL-10 in serum, and MDV load in spleen were determined. The results showed that the treatments with STS and ABOB could significantly increase stimulating index (SI) of peripheral T lymphocytes while the SI is dropping due to the MDV infection, SI of chickens in STS prevention groups were significantly higher than that in STS treatment group and ABOB group (P<0.05 or P<0.01); IFN-γ and IL-10 level of chickens in STS groups were higher than that in other groups (P<0.05 or P<0.01). The results of qPCR demonstrated that STS could inhibit the virus replication in spleen of chickens infected with MDV. These findings indicated that STS can be potentially applied as an anti-MDV drug and set a solid basis for further investigating the antiviral mechanisms of STS.