科研之友
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摘要
Tumor Necrosis Factor (TNF)-alpha is a proinflammatory cytokine (PIC) and has been implicated in a variety of illness including cardiovascular disease. The current study investigated the inflammatory response trigged by TNF alpha in both cultured brain neurons and the hypothalamic paraventricular nucleus (PVN), a key cardiovascular relevant brain area, of the Sprague Dawley (SD) rats. Our results demonstrated that TNF alpha treatment induces a dose- and time-dependent increase in mRNA expression of PICs including Interleukin (IL)-1 beta and Interleukin-6 (IL6); chemokines including C-C Motif Chemokine Ligand 5 (CCL5) and C-C Motif Chemokine Ligand 12 (CCL12), inducible nitric oxide synthase (iNOS), as well as transcription factor NF-kB in cultured brain neurons from neonatal SD rats. Consistent with this finding, immunostaining shows that TNF alpha treatment increases immunoreactivity of IL1 beta, CCL5, iNOS and stimulates activation or expression of NF-kB, in both cultured brain neurons and the PVN of adult SD rats. We further compared mRNA expression of the aforementioned genes in basal level as well as in response to TNF alpha challenge between SD rats and Dahl Salt-sensitive (Dahl-S) rats, an animal model of salt-sensitive hypertension. Dahl-S brain neurons presented higher baseline levels as well as greater response to TNF alpha challenge in mRNA expression of CCL5, iNOS and IL1 beta. Furthermore, central administration of TNF alpha caused significant higher response in CCL12 in the PVN of Dahl-S rats. The increased inflammatory response to TNF alpha in Dahl-S rats may be indicative of an underlying mechanism for enhanced pressor reactivity to salt intake in the Dahl-S rat model.
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单位广州中医药大学
