[Changes of cytokine and nuclear factor-kappa B in acute paraquat poisoned rats].
OBJECTIVE
To observe the changes of cytokine and NF-kappaB activity in acute paraquat poisoned rats and the effect of PDTC and the mechanism of lung injury caused by paraquat poisoning.


METHODS
Sprague-Dawley (SD) rats were randomly divided into three groups: Control group (6 rats), PQ group (56 rats) and PQ + PDTC group (46 rats). On the 1st, the 3rd, the 7th, the 14th, the 28th and the 56th day after treatment, the level of interleukin-1 beta (IL-1 beta), tumor necrosis factor-alpha (TNF-alpha), transforming growth factor-beta 1 (TGF-beta1) and platelet-derived growth factor (PDGF) in serum were detected; the activity of NF-kappaB in lung tissues was detected.


RESULTS
The level of IL-1 beta increased significantly on the 1st, the 3rd, the 7th day in PQ group compared with control group (P<0.01). The content of TGF-beta1 and TNF-alpha in PQ group significantly increased compared with control group (P<0.05 or P<0.01). The level of PDGF significantly increased on the 7th, the 14th, the 28th and the 56th day compared with control group (P<0.01). Meanwhile, IL-1 beta and TNF-alpha were positively correlated with lung coefficient (r=0.37, 0.46, P<0.05 or P<0.01 ); TGF-beta1 and PDGF had positive correlation with hydroxyproline (r=0.56, 0.89, P<0.01). The activity of NF-kappaB in lung tissue of PQ group significantly increased on the 1st, the 3rd, the 7th and 14th day compared with control (P<0.05 or P<0.01). There was a significant decrease of IL-1 beta, TGF-beta1, TNF-alpha and PDGF in PQ + PDTC group compared with PQ group (P<0.05 or P<0.01) in the corresponding sacrifice dates. There was a significant decrease in NF-kappaB activity on the 1st, the 3rd, the 7th day in PQ + PDTC group compared with PQ group (P<0.01).


CONCLUSIONS
The cytokine and NF-kappaB could play an important role in lung injury of poisoned rats. PDTC may inhibit the expression of NF-kappaB and further reduce the production of cytokines, alleviate lung injury in acute paraquat poisoned rats.
Huang
Min
M
School of Public Health, Fudan University/National Key Laboratory for Public Health and Safety of MOE, Shanghai 200032, China.
Zhang
Ping
P
Chang
Xiu-li
XL
Gu
Xi-an
XA
Wu
Qing
Q
Zhou
Zhi-jun
ZJ
D000818:Animals; D053583:Interleukin-1beta / Q000378:metabolism; D008168:Lung / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D008297:Male; D016328:NF-kappa B / Q000378:metabolism*; D010269:Paraquat / Q000633:toxicity*; D051381:Rats; D017207:Rats, Sprague-Dawley; D053773:Transforming Growth Factor beta1 / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
D053583:Interleukin-1beta; D016328:NF-kappa B; D053773:Transforming Growth Factor beta1; D014409:Tumor Necrosis Factor-alpha; D010269:Paraquat