Protective effect of baicalin solid dispersion on D-galactosamine induced acute hepatic injury in mice / 中国中西医结合杂志

<p><b>OBJECTIVE</b>To study the protective effect of baicalin solid dispersion (BSD) on D-galactosamine (D-GalN) induced acute hepatic injury in mice, and to compare it with baicalin alone.</p><p><b>METHODS</b>Sixty mice were randomly divided into six groups, i.e., the normal control group, the D-GalN model group, the bifendate group (at the daily dose of 200 mg/kg), the baicalin group (at the daily dose of 50 mg/kg), the low dose BSD group (at the daily dose of 50 mg/kg), and the high dose BSD group (at the daily dose of 100 mg/kg), 10 in each group. 0.5% CMC-Na at 20 mL/kg was administered to mice in the normal group and the model group by gastrogavage, while corresponding medication was administered to mice in the other three groups by gastrogavage. Seven days after administration, acute hepatic injury model was induced by intraperitoneal injection of D-GalN. The liver index and the spleen index were calculated. The serum activities of alanine aminotransferase (ALT) and asparate aminotransferase (AST), the contents of superoxide dismutase (SOD) and malondialdehyde (MDA) in the liver homogenate were measured. The pathological changes of the liver tissue were observed by HE staining.</p><p><b>RESULTS</b>Compared with the normal control group, widespread inflammation and necrosis was significant in the liver tissue of the D-GalN model group; the liver index, serum ALT and AST levels and hepatic MDA content obviously increased, hepatic SOD activity decreased, showing statistical difference (P < 0.05). Compared with the model group, the liver index, the serum levels of ALT and AST, and hepatic MDA decreased, hepatic SOD increased, the degree of hepatic tissue injury was significantly improved in the low dose and high dose BSD groups. Besides, better effects were obtained in the low dose BSD group than in the baicalin group with statistical difference (P < 0.05).</p><p><b>CONCLUSION</b>BSD could significantly protect D-GalN induced acute hepatic injury of mice, and its effect was superior to that of baicalin alone.</p>

Sodium butyrate inhibits HMGB1 expression and release and attenuates concanavalin A-induced acute liver injury in mice / 生理学报

The purpose of the present study is to explore the protective effects of sodium butyrate (SB) pretreatment on concanavalin A (Con A)-induced acute liver injury in mice. The model animals were first administered intraperitoneally with SB. Half an hour later, acute liver injury mouse model was established by caudal vein injection with Con A (15 mg/kg). Then, levels of serous alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were measured using standard clinical method by an automated chemistry analyzer, tumor necrosis factor-α (TNF-α) and interferon-γ (IFN-γ) were measured by ELISA, and pathological changes in hepatic tissue were observed by using HE staining and light microscopy. The expression and release of high-mobility group box 1 (HMGB1) were assessed by using reverse transcription polymerase chain reaction (RT-PCR), immunohistochemistry and ELISA. The results showed that the pretreatment of SB significantly protected Con A-treated mice from liver injury as evidenced by the decrease of serum ALT, AST (P < 0.01) and reduction of hepatic tissues necrosis. SB also decreased levels of serous TNF-α and IFN-γ (P < 0.01). Furthermore, the expression and release of HMGB1 were markedly inhibited by SB pretreatment (P < 0.05 or P < 0.01). These results suggest that the attenuating effect of SB on Con A-induced acute liver injury may be due to its role of reducing the TNF-α and IFN-γ production, and inhibiting HMGB1 expression and release.

Multi-gene methylation detection increases positive methylation rate in colorectal cancer / 中华胃肠外科杂志

<p><b>OBJECTIVE</b>To study whether combined detection of the methylation status of vimentin, sFRP1, and HPP1 gene can increase the positive methylation rate in colorectal cancer.</p><p><b>METHODS</b>Tissue samples were collected from 90 patients with colorectal cancer, 60 patients with adenomatous polyp, and 20 healthy controls. DNA was extracted and the methylation status of vimentin, sFRP1, and HPP1 gene was detected by Methylation-specific PCR (MSP). The relationship between clinicopathologic features of colorectal cancer and gene methylation was analyzed.</p><p><b>RESULTS</b>The methylation rates of vimentin, sFRP1, and HPP1 were 66.7%, 68.9%, and 72.2% in colorectal cancer, 53.3%, 55.0%, and 50.0% in colorectal adenomas, and 0, 0, and 5.0% in healthy controls, respectively. The methylation of each of the three genes in colorectal cancer tissues was higher than colorectal adenomas and healthy controls(P<0.05). The diagnostic sensitivity by combining three methylation markers was 93.3% in colorectal cancer, 76.7% in colorectal adenomas, which was higher than the sensitivity using single gene testing(P<0.05). No significant associations existed between the methylation status of the three genes and clinical characteristics including sex, age, tumor location, lymph node metastases, distant metastasis, and TNM stage(P>0.05).</p><p><b>CONCLUSIONS</b>DNA methylation levels of vimentin, sFRP1 and HPP1 are significantly higher in colorectal cancer tissue. Combined detection significantly improves the positive rate of methylation, and may be used as early diagnosis method for colorectal cancer.</p>

Expression of 11β-hydroxysteroid dehydrogenase type 2 in lymphoblastic cells and its relationship with glucocorticoid sensitivity / 中国实验血液学杂志

This study was aimed to explore the expression of 11β-hydroxysteroid dehydrogenase type 2 (11β-HSD2) in 3 different lymphoblastic cell lines with relation to their glucocorticoid (GC) sensitivity. The 11β-HSD2 expressions in acute lymphoblastic leukemia Jurkat cells, lymphoma Daudi and Raji cells, and peripheral blood T cells of a healthy volunteer were analyzed by real time PCR and Western blot. Glucocorticoid (GC)-induced apoptosis in 3 different cell lines was detected by flow cytometry. Cell growth in Jurkat cells treated with cortisol was analyzed by trypan blue dye exclusion. Flow cytometry was performed to observe GC-induced apoptosis in Jurkat cells treated by combination of GC with 11β-HSD2 inhibition 18β-glycyrrhetinic acid (18β-GA). The results demonstrated that 11β-HSD2 highly expressed in Jurkat cells, but not in Daudi, Raji cells and normal blood T cells. Compared to Daudi and Raji cells, Jurkat cells were more resistant to GC-induced apoptosis. Furthermore, the inhibition of 11β-HSD2 by 18β-GA resulted in increased cellular sensitivity to GC as shown by elevated induction of apoptosis. it is concluded that 11β-HSD2 is at least partly responsible for GC resistance in Jurkat cells. 11β-HSD2 may be a potential target for reduction of GC-resistance in therapeutic applications.

Expression of transcription factor LYL1 in leukemia and its possible role in leukemogenesis / 中华血液学杂志

<p><b>OBJECTIVE</b>To study the expression of transcription factor LYL1 in leukemia and its possible role in leukemogenesis.</p><p><b>METHODS</b>Fluorescence real time quantitative polymerase chain reaction was used to detect the expression levels of LYL1 in leukemias. Specific siRNA was used to silence the expression of LYL1 in K562 cells.</p><p><b>RESULTS</b>Compared to CD34 positive cells from normal bone marrow, the expression of LYL1 was significantly elevated in patients with acute myeloid leukemia (AML) and acute lymphoblastic leukemia (ALL). LYL1 expression was higher in chronic myeloid leukemia (CML) in blastic crisis than that in chronic phase (7.831 vs 1.672, P < 0.01). LYL1 expression in AML in complete remission (CR) was down-regulated as compared with that of un-remission patients (1.400 vs 9.985, P < 0.01). Down-regulation of endogenous expression of LYL1 in K562 cells by a combination of three specific siRNA could inhibit cellular growth and clonogenicity to some extent.</p><p><b>CONCLUSION</b>Over-expression of LYL1 is highly associated with AML as well as ALL. RNA interference targeting specific oncogenes such as LYL1 is potentially useful in the treatment of hematological malignancies.</p>

Effect of earthworm decoction on airway inflammation of bronchial asthma in guinea pigs / 中国中药杂志

<p><b>OBJECTIVE</b>To investigate the effect of Earthworm decoction on the airway inflammation of experimental bronchial asthma in guinea pigs and inquire into the mechanism in the decoction.</p><p><b>METHOD</b>Forty-eight guinea pigs were randomly divided into six groups: the control group, the model group, the dexamethasone group, the Xiaoqinglong decoction group, the earthworm decoction large dosage group and the Earthworm decoction low dosage group, 8 guinea pigs in each group. Except the control group, the other groups were sensitized with ovalbumin (OVA) by a combination of intraperitional injection and repeated intranasal challenges to establish the guinea pigs asthma model. However, in the control group, normal saline was used. The morphological changes of bronchial tube, the lung tectology and the inflammation germ cell quantity of eosinophils (Eos), lymphocytes (Ly), neutrophils (Neu) and total blood cells in the blood and bronchoalveolar lavaga fluid (BALF) were examinated in each group respectively.</p><p><b>RESULT</b>The levels of Eos, Ly, Neu and total cell quantity in the blood and BALF after the earthworm decoction treatment in the large dosage group were significantly lower than those in the model group (P <0.01), and in the low dosage group were lower too (P <0.05). The Earthworm decoction large dosage could obviously improve the bronchial tube epidermis damage, the mucous membrane gland proliferation and hydrops, asthma pathology change and basilar membrane accumulation. Eos apoptosis was obsered in the bronchoalveolar, blood and BALF. The Earthworm decoction small dosage had a similar effect but slightly to the large dosage.</p><p><b>CONCLUSION</b>The Earthworm decoction can lighten the airway inflammation in asthmatic guinea pigs, its mechanism is related with the inhibition of Eos infiltration, acceleration of Eos apoptosis and improvement of the bronchial tube and the lung tectology changes. The effect of the decoction is dose-dependent.</p>