RESUMO
OBJECTIVE: To explore the effect of oxymatrine (OMT) on JAK2/STAT3 signaling in renal tissues of rats with septic shock. METHOD: The cecal ligation and puncture (CLP) was adopted to establish the rat septic shock model. Fifty-six male SD rats were randomly divided into 7 groups: the sham operation group, the model (CLP) group, CLP + OMT high, middle, low-dose (52, 26, 13 mg x kg(-1), vena caudalis bolus) groups and the positive control (CLP + dexamethasone, 10 mg x kg(-1)) group. The pathological changes in renal tissues were examined with lightmicroscope. BUN content was determined by urine enzymatic method. Expressions of tumournecrosis factor-alpha (TNF-alpha) and interleukin-1beta (IL-1beta) mRNA in renal tissues were determined by RT-PCR. Expression of JAK2 and STAT3 in renal tissues determined by Western blot. Changes in tumournecrosis factor-alpha (TNF-alpha) and interleukin-1beta (IL-1beta) contents in renal tissue were determined by radioimmunoassay. RESULT: OMT of different doses could inhibit the JAK2 and STAT3 activation in renal tissues (P<0.05), and decrease the protein expression of JAK2, STAT3, TNF-alpha and IL-1beta mRNA (P<0.05). Besides, it could reduce TNF-alpha and IL-1beta contents in renal tissue homogenate (P<0.05), serum BUN content (P<0.05), and improve such lesions as tissue hyperemia, edema and inflammatory cell infiltration, with identical results in medium and high-dose OMT groups, and the positive control group. CONCLUSION: OMT can inhibit JAK2/STAT3 signaling activity to reduce the expression of proin-flammatory factors (TNF-alpha, IL-1beta) and treat the renal injury in rats with septic shock.
Assuntos
Alcaloides/farmacologia , Janus Quinase 2/metabolismo , Rim/efeitos dos fármacos , Rim/patologia , Quinolizinas/farmacologia , Fator de Transcrição STAT3/metabolismo , Choque Séptico/patologia , Transdução de Sinais/efeitos dos fármacos , Animais , Regulação da Expressão Gênica/efeitos dos fármacos , Interleucina-1beta/genética , Interleucina-1beta/metabolismo , Rim/metabolismo , Masculino , Ratos , Ratos Sprague-Dawley , Choque Séptico/sangue , Choque Séptico/metabolismo , Fator de Necrose Tumoral alfa/genética , Fator de Necrose Tumoral alfa/metabolismoRESUMO
OBJECTIVE: To study the effect of anti-atherosclerosis of Lycium Seed Oil (Lso) and its possible mechanism. METHODS: The rabbit atherosclerosis model was established by high fat diet, and the TC, TG, LDL-C, HDL-C levels in plasma were examined dynamically. The SOD, GSH-PX, T-AOC activities and the MDA levels in serum were monitored after 8 week's high fat diet. Aorta samples were observed for atherosclerotic extent, and NF-kappaB, TNF-alpha were assessed by immuno-histochemical method. The lovastatin was set up as a positive control. RESULTS: contents of HDL-C obviously increased in Plasma of low and high dosage groups and TC, TG, LDL-C levels significantly decreased compared with control group. The SOD, GSH-PX, T-AOC activities up-regulated while the NF-kappaB, MDA and NF-alpha levels decreased in Lycium Seed Oil groups compared with control group. Aortic atherosclerotic extent and area in low dosage and high dosage LSO groups were absolutely smaller than that in high fat diet group. The anti-atherosclerosis potency of Lycium Seed Oil was similar with that of lovastatin. CONCLUSION: Lycium Seed Oil has potent anti-atherosclerosis effects and its anti-atherosclerosis potency was similar with The lovastatin. The possible mechanism involve the decreasing of plasma lipids, anti-peroxidation, inhibiting the activation of NF-kappaB and down-regulating the inflammation cytokines of TNF-alpha.