Sinomenine promotes paired immunoglobulin-like receptor B expression to restrain macrophage classic activation / 药学学报

In this study, in vitro experiments were conducted to investigate that sinomenine inhibits the macrophage classic activation by up-regulating the expression of paired immunoglobulin-like receptor B (PIR-B). A macrophage model with classic activation was established by lipopolysaccharide and interferon-gamma co-stimulation. Real-time fluorescence reverse transcription-polymerase chain reaction was executed for evaluating the PIR-B gene expression, and Western blot for PIR-B protein expression, in macrophages, respectively. The tumor necrosis factor α and interleukin 8 in cell culture supernatant were measured by enzyme-linked immunosorbent assay. The flow cytometry was utilized to detect M1 macrophages. The PIR-B expression in situ was observed by laser scanning confocal microscope. The results showed that sinomenine significantly increased the expression of PIR-B, markedly reduced the percentage of M1 macrophages, and decreased the levels of tumor necrosis factor α and interleukin 8 in the culture supernatant. The above results indicated that sinomenine can significantly inhibit the macrophage classic activation, and its mechanism may be related to the increase of PIR-B expression in macrophages. This pharmacological effect helps explain the pharmacodynamic mechanism of sinomenine in treating rheumatoid arthritis.

Effect of Wuzang Wenyang Huayu Decoction on Neurofibrillary Tangles by Inhibiting Cyclin-dependent Kinase-5 Over-expression in SAMP8 Mice / 中国实验方剂学杂志

Objective: To explore the mechanism of Wuzang Wenyang Huayu decoction in improving the cognitive competence and the pharmacological mechanism for neurofibrillary tangles related to cyclin-dependent kinase-5(CDK-5).Method: The 10 SAMR1 mice were used as normal group,40 SAMP8 mice were randomly divided into model group,donepezil group (0.4 mg·kg-1·d-1),high and low dose Wuzang Wenyang Huayu decoction groups (5,1.25 g·kg-1·d-1).Drugs were administered by gastric lavage for 4 continuous weeks.Directional navigation and space exploration ability were evaluated with Morris amaze.Real-time PCR was used to measure the mRNA expression of CDK-5 in brain nerve tissues.Western blot was used to detect the protein expression of CDK-5 and phosphorylation of Tau protein.Meanwhile,neurofibrillary tangles in brain tissue were detected with silver staining method.Result: As compared with normal group,both CDK-5 expression and Tau protein phosphorylation in brain nerve tissues were remarkably increased in model group (PPPPPPConclusion: Wuzang Wenyang Huayu decoction can markedly improve the cognitive competence of SAMP8 mice,and the mechanism may be related to its inhibition on CDK-5 over-expression,and down-regulation of Tau protein phosphorylation and neurofibrillary tangles in brain tissue.

Effect of mangiferin on superoxide dismutase isozyme expression in rats with chronic bronchitis / 中国药学杂志

OBJECTIVE: This research was designed to investigate the regulation of mangiferin on superoxide dismutase (SOD) isozyme expressionin rats with cigarettesmoke-induced chronic bronchitis, plus withthe protection on bronchial epithelial cellsultrastructure and anti-inflammatory action. METHODS: The rat model with chronic bronchitis was established by cigarette smoke. Real-time fluorescence RT-PCR was executed for evaluating the SOD1, SOD2 and SOD3 gene expression in lung tissue, and enzyme-linked im-muno sorbent assay (ELISA) for SOD1, SOD2 and SOD3 protein level. As well, interleukin-1 (IL-1), tumor necrosis factor-a (TNF-a) and malondialdehyde (MDA) level in lung tissue were detected by ELISA. Furthermore, the bronchial epithelial cellsultrastructure was observed under transmission electron microscopy. The histopathological images was obtained by lung tissue HE staining slides. RESULTS: The cigarette smokeresulted in a markedly down-regulation expressions of SOD1, SOD2 and SOD3 in lung tissue. The down-regulation expressions of SOD1 and SOD2 in lung tissue cannot be antagonized by mangiferin. However, mangiferin significantly inhibited the down-regulation of SOD3, and markedly decreased IL-1, TNF-a and MDA. Furthermore, the structural completeness of the bronchial epithelial cellsultrastructure was maintainedin a good attitude by mangiferin, while the greatly reduced chronic bronchitis was found. CONCLUSION: Mangiferin can obviously reduce the chronic bronchitis induced by cigarette smoke and keep the bronchial epithelial cells from damage. The protective action might not rely only on anantagonistic action on down-regulated SOD3 expression in lung tissue by mangiferin.

Mangiferin protects rats against chronic bronchitis via regulating NF-kappaB (P65) and IkappaBalpha expression in mononuclear cells / 药学学报

This study is to investigate the protective effect of mangiferin on NF-kappaB (P65) and IkappaBalpha expression in peripheral blood mononuclear cell (PBMC) in rats with cigarette smoke induced chronic bronchitis. The rat model with chronic bronchitis was established by cigarette smoke. Real-time fluorescence RT-PCR was executed for evaluating the NF-kappaB (P65) and IKkappaBalpha gene expression in mononuclear cell, and flow cytometry for their protein expression. The serum hs-CRP (high-sensitivity C-reactive proteins) and TNF-alpha (tumor necrosis factor-alpha) were detected by enzyme-linked immunosorbent assay. The histopathological score was obtained from lung tissue HE staining slides of lung tissue. The results showed that mangiferin could markedly suppress the NF-kappaB (P65) mRNA and protein expression in mononuclear cell, while promote the IkappaBalpha mRNA and protein expression. Furthermore, mangiferin could lower serum hs-CRP and TNF-alpha level, and reduce the chronic inflammatory damage of bronchiole. These results suggested that mangiferin could notably ameliorate chronic bronchiole inflammation induced by cigarette smoke, and this protective effect might be linked to the regulation of NF-kappaB (P65) and IkappaBalpha expression in mononuclear cell.