[Effect and mechanism of bamboo leaf flavonoids on depression in type 2 diabetic rats].

Objective: To explore the effect and mechanism of bamboo leaf flavonoids on depression in type 2 diabetic rats. Methods: The streptozotocin (STZ) was used to induce the depression model of type 2 diabetic rats. Eight weeks old male Sprague-Dawley (SD) rats were randomly divided into 5 groups: the normal control group (n=8), the model group (n=9), the bamboo leaf flavonoid group (n=9), the solvent control group (n=9) and the bamboo leaf flavonoid normal control group (n=8). Rats of the bamboo leaf flavonoid group and the bamboo leaf flavonoid normal control group were treated with intragastric administration of bamboo leaf flavonoids (200 mg·kg(-1)·d(-1)) for 12 weeks. Tail suspension test (TST) and forced swimming test (FST) were used to measure the level of depression. Nissl staining was used to detect the survival amount of hippocampus neurons. The levels of interleukin-1ß (IL-1ß) and interleukin-6 (IL-6) were detected by enzyme-linked immunosorbent assay (ELISA). The expression levels of receptor of advanced glycation endproducts (RAGE), phosphorylated signal protein P38 (p-P38), cleaved caspase-3 and the nuclear factor-κB (NF-κB) were detected by Western blotting. Results: Compared with the normal control group, the TST and FST immobility time of the model group rats increased [(206±13) s vs (101±9) s, (192±24) s vs (98±8) s, both P<0.01]. Furthermore, the injury of hippocampal neurons was more severe, and the boundary was unclear. The nissl bodies were scarce or disappeared, and nuclear pyknosis was observed. The levels of hippocampal CA3 IL-1ß and IL-6 elevated [(31.78±4.12) pg/ml vs (9.26±3.52) pg/ml, (49.15±3.47) pg/ml vs (19.63±2.18) pg/ml, both P<0.01]. The Western blotting showed that the expressions of RAGE, p-P38, cleaved caspase-3 enhanced and NF-κB nuclear translocation increased (all P<0.05). After bamboo leaf flavonoids treatment (for 12 weeks), compared with the model group, the immobility time of TST and FST reduced in the bamboo leaf flavonoid group [(152±11) s vs (206±13) s, (110±19) s vs (192±24) s, P<0.01], and hippocampal neuronal injury alleviated. In addition, the concentrations of IL-1ß and IL-6 decreased [(21.79±3.95) pg/ml vs (31.78±4.12) pg/ml, (34.68±4.28) pg/ml vs (49.15±3.47) pg/ml, both P<0.01] and the expressions of RAGE, p-P38, nuclear NF-κB, cleaved caspase-3 up-regulated in the bamboo leaf flavonoid group. Conclusion: Bamboo leaf flavonoids can effectively improve depression in diabetic rats through decreasing hippocampal neuronal injury and the release of inflammatory factors, and inhibiting RAGE/P38/NF-κB signaling pathway.

The study of health effects of vinyl chloride air pollution on population.

A series of indicators, including serum lysozyme activity, G-banding chromosome aberration (G-banding CA) analysis, sister chromatid exchanges (SCEs), chromosome aberration (CA), T-lymphocyte transformation rate (TcTR), gamma-GT, GPT and AKP, were employed in the present survey among occupationally vinyl chloride (VC) exposed workers and inhabitants living in VC polluted area in a polyvinyl chloride (PVC) factory. The results showed that the serum lysozyme (S-LZM) activities in Group 3 (adult inhabitants exposed to 0.20 mg/m3 VC for at least 8 years), Group 2 (workers exposed to 4.1 mg/m3 for at least 7 years occupationally), Group 1 (workers exposed to 25.7 mg/m3 for at least 2 years) were significantly higher than control. G-banding CA analysis showed that the total chromosome breakage rates in both Groups 1 and 2 were higher, but no difference existed between Group 3 and control. Only Group 1 was observed having higher SCEs, CA level and lower TcTR than control. AKP levels in Groups 1 and 2 were higher than control, but no gamm-GT and GPT differences were found among groups. The study also suggests that G-banding CA analysis is more sensitive than CA and SCEs.

Lymphocyte subsets and sister-chromatid exchanges in the students exposed to formaldehyde vapor.

The present report evaluates the effects of formaldehyde (FA) exposure on peripheral lymphocytes by using both genetic and immunological parameters. Twenty-three non-smoking students in the study had inhalation exposure to 0.508 +/- 0.299 mg/m3 of FA for a period of 8 weeks (3h x 3 times each week) during anatomy classes. As for composition of lymphocyte subsets after FA exposure, significant increase was found in the percentage of CD19 (B cells), while significant decrease was observed in CD3 (total T cells), CD4 (T helper-inducer cells), and CD8 (T cytotoxic-suppressor cells) with a P < 0.01. Increase in the ratio of T-helper-inducer cells to T-cytotoxic-suppressor cells (T4/T8) was also observed with statistical significance after exposure (P < 0.001). In the meanwhile, no significant difference (P > 0.05) was reported between lymphocyte proliferation rate and sister-chromatid exchange (SCE) at the exposure level and duration. It is suggested that the lymphocyte subsets may be most susceptible to the effects of FA, though a single immunological endpoint is rarely related with pathophysiological interpretation.

Micronuclei in nasal mucosa, oral mucosa and lymphocytes in students exposed to formaldehyde vapor in anatomy class.

The frequency of micronuclei (MN) in cells of the nasal mucosa, oral mucosa and in lymphocytes was evaluated for 25 students in anatomy classes exposed to formaldehyde (FA) over an 8-week period. Each student served as his or her own control. The time-weighted average concentration (TWA) of formaldehyde in anatomical laboratories and in students' dormitories was 0.508 +/- 0.299 mg/m3 and 0.012 +/- 0.0025 mg/m3, respectively. A higher frequency of micronuclei was observed in nasal and oral exfoliative cells after formaldehyde exposure (3.85 +/- 1.48 vs 1.20 +/- 0.676 and 0.857 +/- 0.558 vs 0.568 +/- 0.317, paired-t test: P < 0.001 and P < 0.01, respectively). No significant increase in the frequency of lymphocyte micronuclei was found after formaldehyde exposure (P > 0.05). The present study shows that nasal mucosa cells exposed through respiration are the chief target of FA-induced genotoxic effects.