Stevioside protects LPS-induced acute lung injury in mice.

Stevioside, a diterpene glycoside component of Stevia rebaudiana, has been known to exhibit anti-inflammatory properties. To evaluate the effect and the possible mechanism of stevioside in lipopolysaccharide (LPS)-induced acute lung injury, male BALB/c mice were pretreated with stevioside or dexamethasone 1 h before intranasal instillation of LPS. Seven hours later, tumor necrosis factor-α, interleukin-1ß, and interleukin-6 in bronchoalveolar lavage fluid (BALF) were measured by using enzyme-linked immunosorbent assay. The number of total cells, neutrophils, and macrophages in the BALF were also determined. The right lung was excised for histological examination and analysis of myeloperoxidase activity and nitrate/nitrite content. Cyclooxygenase 2 (COX-2), inducible NO synthase (iNOS), nuclear factor-kappa B (NF-κB), inhibitory kappa B protein were detected by western blot. The results showed that stevioside markedly attenuated the LPS-induced histological alterations in the lung. Stevioside inhibited the production of pro-inflammatory cytokines and the expression of COX-2 and iNOS induced by LPS. In addition, not only was the wet-to-dry weight ratio of lung tissue significantly decreased, the number of total cells, neutrophils, and macrophages in the BALF were also significantly reduced after treatment with stevioside. Moreover, western blotting showed that stevioside inhibited the phosphorylation of IκB-α and NF-κB caused by LPS. Taken together, our results suggest that anti-inflammatory effect of stevioside against the LPS-induced acute lung injury may be due to its ability of inhibition of the NF-κB signaling pathway. Stevioside may be a promising potential therapeutic reagent for acute lung injury treatment.

Shikonin inhibits the proliferation and induces the apoptosis of human HepG2 cells.

This study investigated the potential of shikonin as an anticancer agent against liver cancer and an in vitro human hepatoma cancer model system. The HepG2 cell line was the hepatoma cancer model in the present study. The inhibitory effect of shikonin on the growth of HepG2 cells was measured by MTT assay. To explore the underlying mechanism of cell growth inhibition of shikonin, the cell cycle distribution, DNA fragmentation, mitochondrial membrane potential (ΔΨm) disruption, and expression of Bax and Bcl-2 were measured in HepG2 cells. The activity of shikonin in inducing apoptosis was investigated through the detection of Annexin V signal and CD95 expression by flow cytometry and electron microscopy, respectively. Shikonin inhibited the growth of HepG2 cells in a dose-dependent manner. The IC50 value (inhibiting cell growth by 50%) was 4.30 mg/mL. Shikonin inhibited cell growth in a dose-dependent manner and blocked HepG2 cell cycle progression at the S phase. The changes in mitochondrial morphology, dose-dependently decreased in ΔΨm, were observed in different concentrations of the drug treatment group. Western blot analysis showed that cajanol inhibited Bcl-2 expression and induced Bax expression. Furthermore, we show that shikonin increases Annexin V signal and CD95 (Fas/APO) expression, resulting in apoptotic cell death of HepG2 cells. In addition, lump formation of intranuclear chromatin, pyknosis of cell nucleus, deletion of microvillus, vacuolar degeneration of mitochondria, reduction of rough endoplasmic reticulum, and resolution of free ribosome, etc., associated with apoptosis were discovered by electron microscopy in HepG2 cells after 48 h treatment. Shikonin inhibited HepG2 cells, possibly through the pathway of inducing early apoptosis, and was beneficial for restoring the apoptotic sensitivity of HepG2 cells by CD95, and should therefore be considered as a candidate agent for the prevention or treatment of human hepatoma.

The expression of Fc?RⅡb and anti-C1q antibodies in systemic lupus erythematosus / 中华风湿病学杂志

Objective To investigate the expression of Fc?RⅡb on peripheral blood mononuclear cells(PBMCs)and serum anti-C1q antibodies in SLE patients and their role in SLE pathogenesis.Methods The ex-pression of Fc?RⅡb on peripheral neutrophiles,lymphocytes and monocytes was detected by flowcytometry and the level of anti-C1q antibodies was tested by ELISA in32SLE patients and22healthy individials.At the same time,the correlation between Fc?RⅡb,anti-C1q antibodies and ANA,anti-dsDNA antibodies,SLEDAI was eval-uated respectively.Results The expression of Fc?RⅡb on peripheral neutrophiles,lymphocytes and monocytes(especially on neutrophiles and monocytes)of SLE patients decreased,the level of anti-C1q antibodies was signifi-cantly increased,compared with that of the control group.Fc?RⅡb was negatively and anti-C1q antibodies were positively associated with ANA,anti-dsDNA antibodies and SLEDAI respectively.Conclusion The defective ex-pression of Fc?RⅡb on PBMCs and high level of anti-C1q antibodies do exist in SLE patients.Fc?RⅡb and anti-C1q antibodies may decrease the clearance of immune complex and play an important role in the pathogene-sis of SLE.They may also be important parameters in indicating SLE activity.