Browsing by Subject "Inflammatory cytokines"

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    Autoantibodies to the Angiotensin Type I Receptor in Response to Placental Ischemia and Tumor Necrosis Factor α in Pregnant Rats
    (American Heart Association, 2008-10-13) LaMarca, Babbette; Wallukat, Gerd; Llinas, Maria Teresa; Herse, Florian; Dechend, Ralf; Granger, Joey P.; Fisiología
    Circulating factors, such as agonistic autoantibodies to the angiotensin II type 1 (AT1) receptor (AT1-AAs), and inflammatory cytokines, including tumor necrosis factor α (TNF-α), are suggested to be important links between placental ischemia and hypertension in preeclamptic women. The purpose of this study was to determine the role of placental ischemia and TNF-α in stimulating the AT1-AA and the importance of AT1 receptor activation in mediating hypertension during reductions in uterine perfusion pressure (RUPP) and chronic TNF-α excess in pregnant rats. Increased mean arterial pressure in RUPP pregnant rats (122±1 mm Hg RUPP versus 101±1 mm Hg normal pregnant [NP]; P<0.001) was associated with increased circulating TNF-α (RUPP 48±13 pg/mL versus N 8±1 pg/mL; P<0.05) and AT1-AA (RUPP 15.3±1.6 U versus NP 0.6±0.3 U; P<0.001). Moreover, TNF-α–induced hypertension (97±2 to 112±2 mm Hg; P<0.05) in pregnant rats was associated with AT1-AA production (TNF-α rats 9.2±2.3 U versus NP rats 1.0±0.8 U; P<0.05). To determine the importance of AT1 receptor activation in mediating hypertension in RUPP– and TNF-α–treated rats, we administered an AT1 receptor antagonist to RUPP–, TNF-α–treated, and NP rats. Blood pressure responses were attenuated in RUPP rats (Δ 32 mm Hg versus Δ 20 mm Hg, NP; P<0.001), as well as in TNF-α–treated rats (Δ 10 mm Hg versus Δ 5 mm Hg, NP; P<0.05). Collectively, these data indicate that placental ischemia and TNF-α are important stimuli of AT1-AA, and activation of the AT1 receptor appears to, in part, mediate hypertension produced by RUPP and TNF-α in pregnant rats.
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    Regulation of inflammatory cytokines for spinal cord injury recovery
    (Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2021) Lin, Sen; Xu, Chang; Lin, Jiaquan; Hu, Hengshuo; Zhang, Chuanjie; Mei, Xifan
    Spinal cord injury (SCI) is one of the most destructive traumatic diseases in human beings. The balance of inflammation in the microenvironment is crucial to the repair process of spinal cord injury. Inflammatory cytokines are direct mediators of local lesion inflammation and affect the prognosis of spinal cord injury to varying degrees. In spinal cord injury models, some inflammatory cytokines are beneficial for spinal cord repair, while others are harmful. A large number of animal studies have shown that local targeted administration can effectively regulate the secretion and delivery of inflammatory cytokines and promote the repair of spinal cord injury. In addition, many clinical studies have shown that drugs can promote the repair of spinal cord injury by regulating the content of inflammatory cytokines. However, topical administration affects only a small portion of inflammatory cytokines. In addition, different individuals have different inflammatory cytokine profiles during spinal cord injury. Therefore, future research should aim to develop a personalized local delivery therapeutic cocktail strategy to effectively and accurately regulate inflammation and obtain substantial functional recovery from spinal cord injury