[Changes of integrin-linked kinase expression on rats' pulmonary fibrosis induced by paraquat].

Objective: To observe the expression of integrin-linked kinase on pulmonary fibrosis of paraquat (PQ) poisoning rats, and to discuss the relationship between ILK with pulmonary fibrosis induced by paraquat. Methods: Forty male Sprague-Dawley (SD) rats were randomly divided into control group and paraquat group, 20 in each group; the PQ group rats were intraperitoneally injected PQ liquid (18 mg/kg) , and the control group rats were injected the same volume of saline; 5 rats of these two groups were respectively sacrificed after 7, 14, 28, 56 days of PQ injection; according to the results of lung biopsy HE staining and Masson staining to observe the lung pathologic changes, measure the value of lung hydroxyproline and the expression of ILK. Results: HE and Masson staining of lung pathological biopsy showed, the 7th day after PQ exposure lung tissue mostly had congestion, edema, inflammatory cells infiltration; the 14th inflammation reduced, fibrosis change appeared gradually; the 28th and 56th showed the lung tissue structure disorder and occurred apparent hydroproline with blue dye in pulmonary interstitium. Compared with control group in the same experiment period, the value of lung hydroxyproline in each experiment period of PQ group increased (P<0.05) , and the value of lung hydroxyproline of PQ group rose with the increasing of the time of PQ poisoning. The expression of ILK mRNA and protein in each experiment period of PQ group was higher than the control group in the same experiment period (P<0.05) ; ILK mRNA and protein of PQ group began to increase on 7 day phase, reached the highest on 28 day phase, and decreased on 56 day phase. Conclusion: The expression of ILK mRNA and protein increased with the lung fibrosis progression of PQ poisoning rats, so ILK could be the key molecule target which induced pulmonary fibrosis of PQ poisoning.

Effects of modified Shoutaiwai recipe on integrin ß3 and leukemia-inhibitory factor in endometrium of controlled ovarian hyperstimulation mice during the implantation window.

We investigated the effects of a modified Shoutaiwai recipe on integrin ß3 and leukemia-inhibitory factor (LIF) in the endometrium of controlled ovarian hyperstimulation (COH) mice during the implantation window. Seventy non-pregnant mice were randomly divided into 3 groups: a traditional medicine (TCM) treatment group (N = 30), an aspirin treatment (N = 30) group, and a control group (N = 10). After the model was successfully established, mice in the drug treatment groups and the control group were respectively treated with the modified Shoutaiwai recipe, aspirin, or 0.9% physiological saline. During the implantation window of mice, the middle segment of the mouse uterus was recovered, and integrin ß3 and LIF expressions in the endometrium were respectively detected using an immunohistological two-step method and reverse transcription-PCR. Expressions of integrin ß3 and LIF in the endometrium of mice in the TCM treatment group were significantly increased compared to aspirin-treated and control mice, and those of aspirin-treated mice were increased compared to the control group. Our modified Shoutaiwai recipe may improve the endometrial receptivity of COH mice by increasing the expression of integrin ß3 and LIF in the endometrium during the implantation window.

Increased lymphocyte DNA strand breaks in rubber workers.

OBJECTIVE: To study the effect of occupational exposure to rubber processing, smoking, and alcohol drinking on lymphocyte DNA damage. SUBJECTS AND METHODS: Of 371 employees (197 men and 174 women) from a rubber factory in Guangzhou, 281 were rubber processing workers from five production sections and 90 were managerial workers. Information on occupational exposure, smoking, and drinking was collected by interviews. Blood samples were taken in the morning by venipuncture. DNA damages were measured by the Comet assay. Possible DNA-protein crosslinks were broken down by proteinase K. Tail moment, measured by Komet 4.0 image analysis software, was the measure of DNA damage. RESULTS: The rubber processing workers had larger tail moment than the managerial workers (Geometric mean, 95%CI) [1. 77microm (1.64-1.90) versus 1.52microm (1.36-1.71), P=0.04]. Both smoking [1.93microm (1.74-2.13) versus 1.59microm (1.47-1.71), P=0. 003] and alcohol drinking [2.21microm (1.87-2.62) versus 1.63microm (1.53-1.74), P<0.001] increased tail moment. Tail moment differed significantly among job categories (F=3.21, P=0.008), the largest was observed in mixers. In the non-smoking and non-drinking workers, rubber processing workers had larger tail moment than managerial workers after adjusting for age (P=0.033). General linear model analysis showed that after adjusting for each other, occupational exposure (P=0.027), smoking (P=0.012), and alcohol drinking (P=0. 013) was associated with larger tail moment, whereas age and gender had no effect. CONCLUSIONS: Occupational exposure to rubber processing, smoking, and alcohol drinking can cause DNA damage.

Lymphocyte DNA damage in cigarette factory workers measured by the Comet assay.

To investigate whether there were separate and combined effects of occupational exposure to tobacco dust and smoking on lymphocyte DNA damage, 148 workers from a cigarette manufacturing factory (107 occupationally exposed to tobacco dust from the production department and 41 unexposed controls who were managerial workers) were included in the study. The Tail Moment (TM) of Comet assay was used to measure DNA damage. The two groups had similar mean age, mean duration of work and smoking prevalence. The exposed workers had a larger TM than that of the controls (mean+/-S.D.: 43.43+/-13. 77 vs. 38.89+/-8.98, p<0.05). Smokers had significantly larger TM than non-smokers (47.25+/-14.02 vs. 38.90+/-10.75, p<0.001). Analysis of variance after adjustment for age and gender showed that occupational exposure and smoking had a significant and independent effect on Tail Moment (p=0.025 and p=0.002, respectively) and there was a significant positive two way interaction between the two factors (p=0.019). Age and gender had no significant effect on TM. The present study suggests that smoking and tobacco dust exposure can induce lymphocyte DNA damage and there is a synergistic effect of tobacco dust exposure and smoking on DNA damage.

Effect of 3,6-dimethamidodibenzopyriodonium citrate on Ca2+ in rabbit platelet in vitro.

AIM: To study the effect of 3,6-dimethamidodibenzopyriodonium citrate (I-65) on the cytoplasmic free Ca2+ ([Ca2+]i) concentration in rabbit platelet. METHODS: Measurement of the cytosolic Ca2+ of platelets in vitro by using Quin 2-AM fluorescence technique. RESULTS: In the presence of CaCl2 1 mmol.L-1, I-65 (10, 20, and 30 mumol.L-1) reduced the rise in [Ca2+]i induced by thrombin and calcimycin from 142 +/- 22 nmol.L-1 and 124 +/- 18 nmol.L-1 to 118 +/- 20, 78 +/- 12, 40 +/- 10 nmol.L-1, respectively and 108 +/- 15, 77 +/- 14, 37 +/- 14 nmol.L-1, respectively. In the presence of egtazic acid 2 mmol.L-1, I-65 (10, 20, and 30 mumol.L-1), reduced the Ca2+ release induced by thrombin from 52 +/- 11 nmol.L-1 to 34 +/- 9, 19 +/- 6, and 11 +/- 5 nmol.L-1, respectively. In addition, I-65 (10, 20, and 30 mumol.L-1) also reduced the Ca2+ influx induced by thrombin from 91 +/- 13 nmol.L-1 to 84 +/- 15, 58 +/- 15, and 28 +/- 19 nmol.L-1, respectively. CONCLUSION: I-65 inhibited not only the Ca2+ release, but also the influx of Ca2+ in activation platelet.