菜薹BrNAP克隆及其在采后叶片衰老中的功能分析

在菜薹(Brassica rapa var. parachinensis)中克隆Br NAP1并分析其功能。Br NAP1编码区全长813 bp,编码270个氨基酸,具有NAP转录因子特有的保守结构域,属于NAP亚家族成员。Br NAP1表达量与叶片衰老程度呈正相关且受ABA诱导表达上调。亚细胞定位试验表明Br NAP1定位于细胞核。互补试验显示Br NAP1能使拟南芥atnap滞绿表型回复至野生型,过表达则能引起采后叶片早衰。双荧光素酶试验表明Br NAP1能够激活Br SAG113表达。这些说明Br NAP1是菜薹采后叶片衰老的正调控基因。

CaSR inhibitor Calhex231 regulates vascular hyporeactivity after traumatic hemorrhagic shock in rats through PTH-AR pathway

AIM To determine whether parathyroid hormone （PTH） and adrenergic receptor （AR） contribute to the effects of calcium-sensing receptor （CaSR） inhibitor Calhex231 （Cal） on vascular hyporeactivity after traumatic hemorrhagic shock in rats. METHODS The effect of Cal on blood PTH level in traumatic hemorrhagic shock rats and the effect of exogenous PTH on the blood pressure in normal and shock rats were observed. The protein expression levels of 2 subtypes of AR， including α₁-AR and β₁-AR， in superior mesenteric artery （SMA） and vascular smooth muscle cells （VSMC） were measured by Western blot. RESULTS The blood level of PTH was significantly increased after traumatic hemorrhagic shock， while Cal significantly decreased the level of PTH （P<0.01）. Exogenous PTH treatment significantly lowered blood pressure in normal rats. Treatment with Cal increased the expression of α₁-AR in SMA after shock （P<0.05）. Exogenous PTH treatment significantly reduced the expression of α₁-AR in VSMC， while Cal antagonized this effect of PTH （P<0.05）. CONCLUSION The CaSR inhibitor Cal improves the vascular hyporeactivity after traumatic hemorrhagic shock in rats through decreasing blood PTH level and up-regulating vascular α₁-AR expression.