## 3 Results
### The Role of cq-9 in Vasorelaxation  
We investigated the vasorelaxation response in aortic rings. We found that 30 nM U46619 caused contraction in aortic rings. Rice extract and cq-9 treatment induced vasorelaxation of both endo the lium-intact or endothelium-denoted aortic rings (Figure 6). Here, rice extract or cq-9 treatment significantly increased vasorelaxation of endothelium-intact aortic rings than endothelium-denuded aortic rings. Furthermore, cq-9 treated aorta showed higher vasorelaxation compared to rice extract treated aorta. To further confirm the vascular relaxation effect of K\({}^{+}\) channel blockers on rice extract or cq-9 induced relaxation, we pretreated with apamin, a blocker of Ca\({}^{2+}\) dependent K\({}^{+}\) channels, or tetraethylammonium (TEA), voltage-sensitive K\({}^{+}\) channel (Kv) inhibitor, for 30 min in endothelium-intact aortic rings. Pretreated apamin (10 nM) and TEA (10 nM) did not alter aorta relaxation of rice extract or cq-9 (Figure 6). To determine whether rice extract or cq-9 relaxes vascular contraction through activation of the nitric oxide/cGMP pathway, we pretreated  
Figure 4: Phenotypic evaluation of transgenic and wild type rice under WBPH stress. Panel (**A**) represents OX-OsCM, a minor symptom that appeared after 30 days of infestation. (**B,C**) Cheongcheong and infection appeared very early, but the pictures taken after 20 days and 30 days, respectively, indicate that the infection increased very rapidly and finally the leaves died. (**D,E**) The spreading rate of infection in OX-OsCM leaf indicated with circles. (**F,G**) The pattern of spreading symptoms in Cheongcheong leaves. (**H–K**) The infection spreading rate after each time point and wild and OX-OsCM leaves differentiated with braces. Arrows in panels (H,I) indicate the initial infection site in Cheongcheong. Wild; Cheongcheong.  
endothelium-intact aortic rings with NG-nitro-L-arginine methylester (L-NAME), a nitric oxide synthase blocker, for 30 min. Rice extract or cq-9 was added cumulatively to elicit relaxation when vascular contraction induced by U46619 (30 nM) reached a plateau. However, pretreatment with L-NAME resulted in significantly inhibited vascular relaxation induced by cumulative addition of rice extract or cq-9 (Figure 6).  
Rice extract or cq-9 inhibit agonist-induced rat platelet aggregation. Rice extract or cq-9 inhibited rat platelet aggregation induced in a dose-dependent manner (from 300 ug/mL to 10 ug/mL) by several agonists, including collagen, ADP and thrombin (Figure 7). We also found that cq-9 extract significantly reduced rat platelet aggregation induced by collagen treatment compared to rice extract (30, 100, 300 ug/mL; \(p<0.01\), \(p<0.05\), \(p<0.01\)).  
Figure 5: Effects of cq-9 on vascular barrier disruption under septic conditions and septic death model. (**A**) Effects of treatment with different concentrations of cq-9 for 6 h on barrier disruption caused by lipopolysaccharide-100 ng/mL, 4 h. (**B**) High mobility group protein 1 (HMBG1), 1 ug/mL, 16 h were monitored by measuring the flux of Evans blue-bound albumin across human umbilical vein endothelial cells (HUVECs). (**C**) Effects of SFN on caecal ligation puncture (CLP)-induced vascular permeability in mice were examined by measuring the amount of Evans blue in peritoneal washings (expressed ug/mouse, n = 5). (**D**) Male C57 BL/6 mice (n = 20) were administered compounds cq-9 at 12 and 50 h after CLP. Animal survival was monitored every 12 h after CLP for 132 h. Control CLP mice and sham-operated mice were administered sterile saline (n = 20). Kaplan–Meier survival analysis was used to determine the overall survival rates vs. CLP-treated mice. However, our human pathogenicity experiments did not show any effect. * Significantly different at the 0.05 level.