We investigated the inheritance of cannibalistic behavior in larvae of the common cutworm, Spodoptera litura. The fact that artificial selection of non-cannibalistic animals over 17 generations resulted in decrease of their cannibalistic behavior is clearly the proof of their inheritance of this behavior. Average frequency of cannibalism in selected larvae (3.2%) was significantly lower than that in non-selected larvae (24.5%). We employed the differential display RT-PCR analysis to evaluate differences in gene expression in the brains between selected and non-selected lines, and identified one gene whose expression was significantly higher in non-selected line larvae than that in selected line larvae. The identified gene with 779 bp was a novel gene without a major sequence homology with any reported genes. This gene was expressed in several tissues, fat body, brain, and hemocytes, among which the highest expression was observed in the brain. Further, the expression of this gene was very low in the brain of normally fed larvae but starvation significantly enhanced its expression only in the non-selected larvae. These results imply the possibility that the gene identified in the present study contributes to initiating cannibalistic behavior of S. litura larvae although the detailed function of this gene is unknown at present.
Here, the mechanism of vasorelaxant Mas receptor (MasR)
expression
elevated by hesperidin in spontaneously hypertensive rats was investigated
in human umbilical vein endothelial cells (HUVECs). HUVECs were cultured
with 1 μM hesperidin for 2 h, following the measurements of
nitric oxide (NO) production and vasomotor-related receptors’
expression. Hesperidin significantly promoted NO production (224.1
± 18.3%, P < 0.01 vs control) in the HUVECs.
Only the MasR expression was upregulated (141.2 ± 12.5%, P < 0.05 vs control), whereas a MasR antagonist did not
alter the hesperidin-induced NO production. When a transient receptor
potential vanilloid 1 (TRPV1) was knocked down by silencing RNA or
Ca2+/calmodulin-dependent kinase II (CaMKII) and p38 mitogen-activated
protein kinase (p38 MAPK) were inhibited, the increased MasR expression
by hesperidin was abrogated. The inhibitions of CaMKII and endothelial
NO synthase (eNOS) abolished the hesperidin-induced NO production.
The structure–activity relationship analysis of flavonoids
demonstrated that the B ring of the twisted flavonoid skeleton with
a hydroxy group at the 3′ position was a crucial factor for
TRPV1 stimulation. Taken together, it was demonstrated that hesperidin
may stimulate TRPV1-mediated cascades, leading to the activation of
two signaling axes, CaMKII/p38 MAPK/MasR expression and CaMKII/eNOS/NO
production in HUVECs.
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