Objective To investigate the relation between serum leptin/tumor necrosis factor-α (TNF-α)and malnutrition in patients with chronic obstructive pulmonary disease (COPD) and stable chronic cor pulmonale (CCP) at high altitude. Methods Totally 162 COPD and CCP patients and 40 normal controls (group C) were studied. COPD and CCP patients were divided into malnutrition group (group A, n = 104) and normal nutrition group (group B, n =58) according to the nutritional parameters. Levels of serum leptin and TNF-α were measured by enzyme-linked immunosorbent assay (ELISA). Results Body mass index (BMI), percentage of normal body weight (NW%), triceps skinfold thickness (TSF), mid-upper arm circumference (MAC), serum albumin (ALB) ingroupA[(17.4±1.8) kg/m2, (82.3±4.3)%, (7.0±2.6) mm, (17.8±2.8) cm, (30.3±3.9)g/L, respectively] were significantly lower than those in group B and group C [(21.8 ± 2.0) kg/m2,(98.6±5.5)%, (9.3±2.6) mm, (21.5±2.9) cm, (36.2±3.8) g/L, and (23.1±2.3) kg/m2,(102.2±5.2)%, (9.7±3.8) mm, (22.1±2.8) cm, (36.8±3.9) g/L, respectively; all P＜0. 01].The levels of serum leptin and TNF-α in group A [(9.5 ±1. 8) ng/ml and (17.3 ±2. 2) ng/ml, respectively]were significantly higher than those in group A and group C [(7.3 ± 2. 0) ng/ml, (13.5 ± 2. 3) ng/ml; and (6. 7 ±2. 3) ng/ml, (12. 8 ±2. 1) ng/ml, respectively; all P ＜0.01). However, they were not significantly different between group A and group B (all P ＞ 0. 05). The level of leptin was negatively correlated with BMI (r=-0.745, P=0. 0005), NW% (r= -0.887, P=0. 0005), TSF (r= -0.725, P=0. 0005), MAC (r= -0. 761, P=0. 0005), serum albumin (r= -0. 558, P=0. 0005) in group A, and was positively correlated with TNF-α (r = 0. 527, P = 0. 0005). Conclusion Serum leptin and TNF-α correlate with malnutrition in patients with COPD and CCP at high altitude.

AIM: To investigate the immune mechanisms for Periplocin from Cortex Periplocae (CPP) in tumor-bearing mice. METHODS: H_(22) tumor-bearing model BALB/c mice were applied to evaluated in vivo immunoregulatory effect of CPP. The influence of different dose CPP (0.25, 0.50 and 1.00 mg/kg) on immune organs in tumorbearing mice were observed. T cell subsets of mice spleen were detected by flow cytometry. MTT assay was used to determine the influence of CPP on lymphocyte proliferation of mice spleen stimulated by ConA. The levels of TNF-α, IL-2 and IL-12 in serum from mice were detected by means of ELISA. RESULTS: Thymus index and spleen index of H_(22) tumor-bearing model control mice became less than that of normal mice (P < 0.05). Compared to both model and normal control groups, thymus index and spleen index of H_(22) tumor-bearing mice treated with CPP increased obviously (P < 0.05). CPP had no influence on the number of CD8~+ T cells, but up-regulated markedly the number of CD3~+, CD4~+ T cells and the ratio of CD4~+/CD8~+ in tumorbearing mice. In CPP-treated mice, the percentage of CD3~+, CD4~+ T cells were not different from normal mice (P<0.05), the ratio of CD4~+/CD8~+ was higher than that of normal mice (P < 0.05). CPP enhanced obviously lymphocyte proliferation of mice spleen induced by ConA, the SI scores were even higher than that of nornal mice. The levels of TNF-α, IL-2 and IL-12 in serum from CPP-treated mice, increased significantly compared to model control group (P<0.05) in a dose-dependent manner, were similar to or higher than that of normal mice. CONCLUSION: CPP protected immune organs of tumor-bearing mice, increased obviously the percentage of CD4~+ and CD4~+/ CD8~+ among the T cell line, and enhanced lymphocyte proliferation of mice spleen significantly, stimulated the production of TNF-α, IL-2 and IL-12. The results suggested that CPP possessed potent immunoregulatory effect.