The effect of bee pollen on serum IgM and IgG concentration was investigated in normal and immunodepressed mice.The levels of serum IgM and IgG in normal NIH mice were 0.80? 0.07mg/ml ( X ? SD ) and 11. 42 ?2. 31 mg/ml respectively. The concentration of IgM and IgG were all markedly lowered in immunodepres-ssed mice induced by cyclophosphamide 100 mg/kg/d sc for 4d,hydro-cortison 100 mg/kg/d sc for 6d,60Co ?-irradiation 600 rads and S-180 tumor-bearing in comparison to normal control, while IgG and IgM content in mice treated with bee pollen ( Pollen of Brassica campes-tris L. ) 10 g/kg/d orally for 1 month were significantly increased.The results showed that the stimulating effect of bee pollen on humoral immunity may be the base of beneficial effect in human being.

Immunoenhancement activity of bee pollen and its acetone extract was studied in normal, sarcoma-180 bearing, cyclophosphamide- and antilymphocyte serum-treated mice.Bee pollen and its acetone extract given orally for 30 days could significantly increase the production of serum anti-SRBC hemolysin (HC50) and the number of spleen plaque forming cells (PFC) in primary response to sheep red blood cell (SRBC) in young and adult mice. The acetone extract of bee pollen could significantly prevent the decrease of HC50) the number of PFC and specific rosette forming cells (SRFC), and the quantitative hemolysin of spleen cells (QHS) against SRBC in S-180 bearing, cyclophosphamide- and antilymphocyte serum-treated mice respectively.These results suggested that bee pollen of Brassica campestris L. and its acetone extract have immune-enhancement activity.

The effect of bee pollen of Brassica campestris L. and its alcohol extract on lipid peroxidation was observed in vivo and in vitro.The results showed that the production of lipid peroxides in normal liver hotnogenate of mice and elevation of production of lipid peroxides induced by cysteine and FeSO4 in homogenate were found to be inhibited significantly by in vitro addition of alcohol extract of bee pollen.The elevation of lipid peroxides in serum and liver in adult mice induced by alloxan 75 mg/kg(iv)or by administration of peroxidized corn oil 0.2 ml/mouse was markedly inhibited by oral administration of bee pollen (10 g? kg-1?d-1)for 20 days as compared with respective control groups.The level of lipid peroxide in geriatric mice was also markedly lowered by oral administration of bee pollen (10 g?kg-1?d-1)for 3 months as compared to non-treated geriatric mice.Based on the above in vitro and in vivo experimental results, it may be suggested that bee pollen and its alcohol extract protect tissues against destruction by lipid peroxides.

To explore the effect of intensive insulin therapy (IIT) on high mobility group box-1/nuclear factor-κB (HMGB1/NF-κB) signaling pathway in severe traumatic brain injury (sTBI) patient with stress hyperglycemia. Methods Sixty-one sTBI patients with stress hyperglycemia [Glasgow coma scale (GCS) ≤ 8, three times of random blood glucose levels > 11.1 mmoL/L, glycosylated hemoglobin (HbA1c) < 0.065] admitted to the Affiliated Huaian No.1 People's Hospital of Nanjing Medical University from July 2015 to October 2017 were enrolled. Patients were divided into IIT group (29 cases, keeping blood glucose at 4.4-7.8 mmol/L) and conventional glycemic therapy (CGT) group (32 cases, keeping blood glucose at 7.8-12.2 mmo/L) according to the random number table method. Before treatment and 1, 7 and 14 days after treatment, the levels of plasma HMGB1 and tumor necrosis factor-α (TNF-α) were measured by enzyme linked immunosorbent assay (ELISA); C-reactive protein (CRP) was determined by automatic biochemical analyzer, and NF-κB p65 gene expression in peripheral blood mononuclear cells was detected by real-time quantitative polymerase chain reaction (PCR). Results Nine patients were withdrawn from the observation because the 4 consecutive blood glucose monitoring did not reach the target value, combined with severe infection, or abandoned the treatment with serious brain damage. Finally, 52 patients were enrolled in the analysis, including 28 in CGT group and 24 in IIT group. The levels of plasma HMGB1, TNF-α, CRP and the expression of NF-κB gene in monocytes of the two groups at 1 day after treatment were significantly higher than those before treatment, and reached the peak value, then gradually decreased. After 7 days of treatment, they were significantly lower than 1 day. The levels of plasma CRP and TNF-α in the IIT group were significantly lower than those in the CGT group [CRP (mg/L): 36.7±4.4 vs. 45.1±6.1, TNF-α (ng/L): 42.4±9.7 vs. 53.2±9.1, both P < 0.05], the level of HMGB1 in plasma and the expression of NF-κB p65 in monocytes were significantly lower than those in the CGT group after 14 days of treatment [HMGB1 (μg/L): 60.1±8.7 vs. 80.5±9.1, NF-κB p65 (ΔCt): 35.8±8.5 vs. 53.5±7.3, both P < 0.05]. Conclusion IIT inhibits the inflammatory response in sTBI patients with stress hyperglycemia through HMGB1/NF-κB pathway.