[Protective effect of sesamin against myocardial injury induced by cadmium chloride in rats].

OBJECTIVE: To investigate the protective effect of sesamin against cadmium chloride (CdCl2)-induced cardiotoxicity in rats. METHODS: Fifty male Wistar rats were randomly assigned to five groups: control group, CdCl2 group, and low-, middle-, and high-dose sesamin groups. The control group was given normal saline. The CdCl2 group and sesamin groups were intraperitoneally injected with CdCl2 (5 mg/kg×2 d), and the low-, middle-, and high-dose sesamin groups were given 20, 40, and 80 mg/kg sesamin, respectively. All treatments lasted for four weeks. ECG was measured by a physiological recorder, and serum myocardial enzyme levels were determined by biochemical assay. The heart was weighed, and heart tissues were used in histopathological examination and determination of malondialdehyde (MDA) level. RESULTS: Compared with the control group, the CdCl2 group showed significantly higher levels of serum CK and CK-MB, an increased heart coefficient, significant ST-segment elevation, and higher level of MDA in myocardial tissue (P < 0.05). Histopathological analysis showed edema of myocardial tissues and cells, myocardial fibers disorder, karyopyknosis, and uneven or deep staining of nuclear chromatin. Different doses of sesamin relieved the myocardial pathological changes induced by CdCl2, and high-dose sesamin was the most effective. The middle- and high-dose sesamin groups showed significantly reduced serum CK and CK-MB levels compared with the CdCl2 group (P < 0.05). The heart coefficient of the high-dose sesamin group (0.19±0.01%) was significantly lower than that of the CdCl2 group (0.21±0.01%) (P < 0.05). Myocardial MDA levels of the three sesamin groups (42.32±4.65, 36.71±5.34, and 33.12±4.62 nmol/mg pro, respectively) were all significantly lower than that of the CdCl2 group (55.87±3.65 nmol/mg pro) (P < 0.05). CONCLUSION: Sesamin can relieve myocardial injury induced by CdCl2, and one possible mechanism is the enhancement of antioxidant capacity of myocardial tissue.

Ambient PM2.5 caused cardiac dysfunction through FoxO1-targeted cardiac hypertrophy and macrophage-activated fibrosis in mice.

Plenty of epidemiological evidences have shown that ambient particulate matter (PM2.5) exposure increased the prevalence of cardiovascular disease, but the potential mechanism has not been known clearly. We established mice models by ambient PM2.5 exposure system to explore the adverse effects of PM2.5 on cardiac function in mice. Forty-eight C57BL/6 mice were randomly divided into 3 groups and exposed to filtered air (FA), unfiltered air (UA) and concentrated PM2.5 air (CA) for 8 or 16 weeks, 6 hours per day, 7 days per week, respectively. The changes of cardiac structure and function, histological analysis and related mechanism were investigated. The main manifestations of cardiac structure were cardiac hypertrophy and fibrosis in a dose- and time-dependent manner after PM2.5 exposure, which led to the decrease of cardiac systolic function. Cardiac hypertrophy in mice might be regulated by PI3K/Akt/FoxO1 signal. Cardiac fibrosis might be attributed to inflammatory infiltration caused by macrophage activation. Consequently, our data indicated that cardiac hypertrophy and fibrosis might be important factors of PM2.5-induced cardiac dysfunction in mice.

[Effect of lead acetate on the apoptosis and the expression of bcl-2 and bax genes in rat brain cells].

OBJECTIVES: To explore the effect of lead acetate on the apoptosis of rat brain neural cells and the relationship between the apoptosis and the bcl-2 as well as bax gene expression. METHODS: Lead acetate was given to SD rats by intraperitoneal injection for 5 days at the dosage of 25, 50 and l00 mg/kg body weight respectively. The rates of apoptosis and the expression of bcl-2 (Bcl-2) and bax (Bax) in neural cells from cerebral cortex, hippocampus and carebellum were measured respectively by flow cytometry (FCM). RESULTS: The rates of apoptosis in neural cells from cerebral cortex, hippocampus and cerebellum in every treatment group were significantly higher than that of control (P < 0.01), and there was a significant dose-response relationship (r = 0.998, 0.989 and 0.997 respectively). The expression of bcl-2 was significantly decreased, whereas bax was significantly increased, in neural cells from cerebral cortex, hippocampus and cerebellum in every lead acetate treatment group (FI) compared with the control group, and there was a significant dose-response relationship (r = -0.886, -0.787 and -0.832 respectively for bcl-2, r = 0.971, 0.988 and 0.991 respectively for bax). The value of Bcl-2/Bax in every treatment group decreased significantly compared with control, and there was a nice dose-response relationship (r = -0.863, -0.829 and -0.999, respectively). Correlation analysis showed that rates of apoptosis were inversely correlated with the expression of bcl-2 (r = -0.750, -0.509, and -0.667, respectively), whereas positively correlated with the expression of bax (r = 0.748, 0.56l, and 0.668, respectively). And there were inverse correlations between the rates of apoptosis and Bcl-2/Bax expression. CONCLUSION: Lead may induce apoptosis in rat brain neural cells through the down regulation of bcl-2 and the up regulation of bax gene expression.

[Effect of castration on restenosis after precutaneous transluminal angioplasty in male rats].

OBJECTIVE: To observe the developing changes of adventitia in restenosis after precutaneous transluminal angioplasty(PTA), and investigate the effect of androgen on restenosis through contrasting the castrated male rat models and its mechanism. METHODS: Models were constructed of castrated male rats and restenosis of the common carotid artery, and specimens were collected at the 3rd, 7th, 14th and 28th day respectively after modeling. Hematoxylin and eosin staining, immunohistochemical staining, and electronic microscopy were performed to observe the condition of restenosis. RESULTS: Proliferating cells occurred in adventitia first and phenotype of adventitial cells was changed at the 3rd day after PTA. The adventitial proliferating index was the highest at the 7th day after PTA, and proliferating migration towards intimal was observed. The proliferating cells mostly occurred in the middle layer and neointima at the 14th day after PTA. The areas of adventitia and neointima were larger and the degrees of restenosis were higher in the castrated rats than in the non-castrated ones at different time points. Take the 14 d group, the adventitial area was[(3,566 +/- 337) micron2 vs (2,751 +/- 401) micron2, P = 0.008], the neointimal area[(3,553 +/- 477) micron2 vs (2,757 +/- 435) micron2, P = 0.025], the restenosis rate[(76 +/- 2)% vs (60 +/- 8)%, P = 0.005], and the proliferating index [(29 +/- 2)% vs (13 +/- 1)%, P < 0.001]. CONCLUSION: Adventitial proliferation and migration contribute to restenosis after PTA; Androgen in rats can physiologically relieve restenosis, probably through intervening in the activation of adventitia.