[The protective effect of chlorophyllin against oxidative damage and its mechanism].

OBJECTIVE: To investigate whether chlorophyllin could protect human umbilical vein endothelial cell (HUVEC) against oxidative damage by inducing the expression of heme oxygenase-1 (HO-1) and to explore the underlying mechanism. METHODS: The cellular protection of chlorophyllin against oxidative damage was detected by cell-survival assay with flow cytometry. The level of free radicals was detected directly by electron spin resonance spectra. The induced expression of HO-1 was shown by RT-PCR, Western blot, immunofluorescence confocal laser microscopy and enzymatic activity test. Whether the activation of PI3K/Akt pathway was involved was detected by Western blot. RESULTS: Chlorophyllin could protect HUVEC against oxidative damage caused by H2O2 via scavenging the excessive free radicals. Chlorophyllin treatment could induce expression of HO-1 in a dose- and time-dependent manner. The activation of PI3K/Akt pathway was required in the induction of HO-1. LY294002, the specific inhibitor of PI3K, could suppress the activation of PI3K/Akt and the induced expression of HO-1 in a dose-dependent manner. CONCLUSIONS: Chlorophyllin shows cellular protection against oxidative damage by counteracting the excessive free radicals. Up-regulation of HO-1 expression plays a pivotal role in the protection of chlorophyllin, while the activation of PI3K/Akt signaling pathway is required in the induction of HO-1.

[Analysis of developing feature of pneumoconiosis].

OBJECTIVE: To get the message about the developing feature of pneumoconiosis by analyzing the data from 353 cases of pneumoconiosis diagnosed in our hospital recent 6 years. METHODS: To analyze the onset age, onset service years and incubation period of 353 cases of pneumoconiosis, especially in silicosis, coal worker's pneumoconiosis and potter's pneumoconiosis. RESULTS: 353 patients referred to 10 species of pneumoconiosis, the silicosis, coal worker's pneumoconiosis and potter's pneumoconiosis were accounted for 28.90%, 43.34% and 15.01% of total pneumoconiosis respectively. Diagnosed patients who began to exposed to dust during 1950's to 1980's accounted for 84.99% of all the diagnosed patients. The onset age, onset service years and incubation period of silicosis, coal worker's pneumoconiosis and potters pneumoconiosis all showed a shorten trend compared each other every decade, especially after 1980's, but excluded potter's pneumoconiosis because of that the ceramics industry switched to other products in Beijing. There was a positive correlation relationship between average onset age and incubation period in three main species of pneumoconiosis mentioned above, but no significant difference could be seen in average promotion years. Additionally, comparing with other type of work, jade machining workers showed such a characteristic as younger onset and short incubation period. CONCLUSION: The development situation of silicosis, coal worker's pneumoconiosis is still no so optimistic, and the strict surveillance and administration especially to the township enterprises with poor production conditions should get further strengthen.

[Dynamic changes of hemorheology in rats after carbon monoxide poisoning].

OBJECTIVE: To investigate the startup detail of circulation dysfunction and its role in the progress of delayed neuropsychologic sequelae (DNS) after carbon monoxide (CO) poisoning with comparison with the model of ischemia-reperfusion. METHODS: The ischemia-reperfusion rat model was established by Pulsinelli-Brierley method, and the CO poisoning rats model by i.p. injected with CO repeatedly respectively, and the rats were identified with DNS following the experiment of pathology and the ethnology. RESULTS: The whole blood viscosity, plasma viscosity, hematocrit and fibrinogen increased significantly immediately after reperfusion, and recovered gradually with the ischemia-reperfusion rat model. The whole blood viscosity decreased significantly immediately after CO treated i.p. Especially at low shear rate, the hematocrit also declined remarkably in the early stage after CO treatment. But 1day later, these parameters turned to the trend of the ischemia-reperfusion rats. There was a prominent elevation of both indexes until the 14th day following CO injection i.p. CONCLUSION: There are significantly sustained hyper-coagulation and hyper-viscosity with circulation in rats after CO poisoning compared with ischemia-reperfusion model during the period of DNS, which might contribute to increase cerebral circulation resistance, blocked blood flow, and deteriorate hypoxemia in progression of DNS.

[Striated muscular injury and myocardiac injury caused by acute carbon monoxide poisoning].

OBJECTIVE: To investigate the incidence of rhabdomyolysis, the relationship between striated muscular injury and myocardiac injury, and the role of elevated serum creatine kinase (CK) played in screening these two complications following acute carbon monoxide poisoning (ACOP). METHODS: 280 patients with ACOP from January 2001 to April 2003 were analyzed retrospectively. According to the clinical manifestations of striated muscular injury (swelling, pain or serious myasthenia), the patients were divided into two groups: the evident injury group and non-evident injury group. RESULTS: The abnormality rate of electrocardiogram (ECG) and cardiac troponin I (CTnI) in the evident injury group (43 patients) were significantly higher than in the non-evident injury group (73.8% vs 43.4%, P < 0.001; 77.8% vs 20.9%, P < 0.001). There was a positive correlation between peak CK and MB isoenzyme (CK-MB) in both groups, respectively (r = 0.819, r = 0.795, P < 0.01). There was no correlation in the evident injury group (P > 0.05) and only negative correlation in the non-evident injury group (r = -0.298, P < 0.01) between peak CK and MB ratio (CK-MB/CK). Multiple regression analysis indicated that peak CK and CK-MB were only related with the striated muscular injury and were not affected by the indexes of the myocardial injury (ECG and CTnI); Both peak CK and CK-MB were positively correlated with the coma time before consultation in the non-evident injury group and the latter was also affected by CTnI. The incidence of positive muscular injury symptoms increased with the elevation of CK activity. There was no significant difference either in the ECG abnormality rate between the < 5 times elevated CK level subgroup and the > 5 times elevated CK level subgroup (P > 0.05), or in the CTnI positive rate between the normal CK level subgroup and the < 5 times elevated CK level subgroup (P > 0.05). CONCLUSION: Striated muscular injury is not a rare complication of ACOP, and always accompanied by myocardial injury. The strikingly elevated serum level of CK in patients with ACOP might be more likely to indicate the striated muscle not myocardiac injury.