RÉSUMÉ
Objective To investigate the toxic effect of hemin on primary cultured neurons,astrocytes,and brain capillary endothelial cells (BCECs),and the damage effect of hemin with different concentrations on the above cells. Methods (1) Primary cultured neurons,astrocytes and BCECs from the cortex of rats were exposed to different doses of hemin for 2 h,and continue culture of these cells for 24 to 96 h after withdrawing hemin was performed; the cellular morphology was examined under phase-contrast microscope; cellular survival rate was measured with Alama blue staining; and the releasing rate of lactate dehydrogenasing (LDH) was detected with regular biochemical method. (2) Primary cultured cells were exposed to different doses of hemin for 2 h,and continue culture of the cells for 4 h was performed after washing out the hemin; and then,concentrated formic acid was employed to dissociate the cells, and heme content in dissociated cells was measured with spectrophotometer. (3) Primary cultured cells was exposed to different doses ofhemin for 30,60 and 120 min,respectively,and continue culture of the cells for 4 h was performed after washing out hemin; and then,intracellular Fe3+was examined with Prussian blue staining. Results (1) Cultured neurons were injured by a low dose ofhemin (5 mmol/L) with a decreased survival rate by 40.2％ and an increased LDH releasing rate by 22.2％; and the pathological changes of cellular morphology were severe after 24 h of exposure to hemin.Following the increased doses ofhemin and time of post-exposure,the cellular death and LDH releasing were increased,and the morphological changes of cells were much severe. (2) The low and medium doses of hemin (5 mmol/L and 25 mmol/L) did not induce cellular death, LDH releasing and morphological changes in astrocytes; and a high dose ofhemin (50 mmol/L) could induce a death rate of astrocytes decreasing by 52.4％, a LDH releasing rate increasing by 31％ and obvious morphological changes of astrocytes; however, the injured astrocytes could regenerate fluent cellular monolayer 96 h after exposing to high dose of hemin treatment.(3) Hemin with either low or high dose did not induce any changes in cellular survival,LDH releasing and cellular morphology of BCECs.(4) The heme content in cultured neurons was significantly higher than that in astrocytes and BCECs after hemin treatment for 2 h.(5) The blue Fe3+ stained granules appeared in neurons as early as 30 min after neurons being exposed to hemin, and Fe3+ stained positive cells in neurons were significantly higher than those in astrocytes and BCECs at any dose ofhemin and any time point ofhemin treatment. Conclusion Hemin is highly toxic to neurons, but it can only injure astrocytes at a high dose and it can not induce direct damage in BCECs; free hemin could rapidly enter and accumulate in neurons,but less accumulate in astrocytes and not accumulate in BCECs.
RÉSUMÉ
<p><b>OBJECTIVE</b>To investigate the effect of Shuganlipi decoction on Th1/Th2 cytokines, liver function and HBV replication in patients with chronic hepatitis B (CHB).</p><p><b>METHODS</b>Eighty-six confirmed CHB cases were randomly divided into control group (n=42) and experimental group (n=44) for treatment with routine western medication and additional treatment with Shuganlipi decoction, respectively. The production of IFN-γ, IL-2, IL-6, IL-10 and liver function, HBV DNA, and HBeAg were detected in all the patients.</p><p><b>RESULTS</b>The total response rate to the treatment was significantly higher in the experimental group than in the control group (78.13% vs 57.14%, P<0.01). ALT, AST, TBIL and ALB were all improved obviously in the two groups after the treatments (P<0.01). In terms of ALT and ALB, the experimental group showed more obvious improvement than the control group(P<0.05). The treatments also resulted in significant increases of IFN-γ and IL-2 levels and reductions of IL-6 and IL-10 levels in the two groups (P<0.01).</p><p><b>CONCLUSION</b>Shuganlipi decoction can improve the liver function and activity of Th1/Th2 cytokines to promote the clearance of liver cell HBV infection.</p>