Abstract：
BACKGROUND: C1q/TNF-related protein 9 (CTRP9) and adiponectin (APN) have beneficial metabolic regulatory and vasoprotective effects. This study explored alteration of CTRP9 and APN multimers during onset of ischemic stroke and development, to provide novel clinical and experimental basis for recognition and prevention of ischemic stroke.
METHODS: There were 269 patients with ischemic stroke and 182 control subjects included in this study. Serum levels of CTRP9 and APN multimers in different disease stages were measured.
RESULTS: Serum CTRP9, total APN (tAPN), and high-molecular weight (HMW) APN decreased gradually in stage I (acute stage, within 72 h of onset) of ischemic stroke and increased during stage III (11th day to one month) and stage IV (1 month after), compared to control. In the non-hyperlipidemia group, serum CTRP9, tAPN, and HMW were decreased in ischemic stroke patients compared to control (P < 0.05). Serum CTRP9 is closely related to serum tAPN and HMW (r = 0.992, 0.991). Serum CTRP9 are protective against ischemic stroke (OR = 0.400, 95% CI 0.197-0.810, P < 0.05).
CONCLUSIONS: Lower serum CTRP9, tAPN, LMW, and HMW are significantly associated with increased ischemic stroke risk in non-hyperlipidemia subjects. CTRP9, tAPN, and HMW isoforms may be valuable clinical indicators for patients with ischemic stroke.
METHODS: There were 269 patients with ischemic stroke and 182 control subjects included in this study. Serum levels of CTRP9 and APN multimers in different disease stages were measured.
RESULTS: Serum CTRP9, total APN (tAPN), and high-molecular weight (HMW) APN decreased gradually in stage I (acute stage, within 72 h of onset) of ischemic stroke and increased during stage III (11th day to one month) and stage IV (1 month after), compared to control. In the non-hyperlipidemia group, serum CTRP9, tAPN, and HMW were decreased in ischemic stroke patients compared to control (P < 0.05). Serum CTRP9 is closely related to serum tAPN and HMW (r = 0.992, 0.991). Serum CTRP9 are protective against ischemic stroke (OR = 0.400, 95% CI 0.197-0.810, P < 0.05).
CONCLUSIONS: Lower serum CTRP9, tAPN, LMW, and HMW are significantly associated with increased ischemic stroke risk in non-hyperlipidemia subjects. CTRP9, tAPN, and HMW isoforms may be valuable clinical indicators for patients with ischemic stroke.
摘要：
背景：C1q/TNF相关蛋白9（CTRP9）和脂联素（APN）具有有益的代谢调节和血管保护作用。这项研究探讨了CTRP9和APN多聚体在缺血性中风发作和发展过程中的变化。为缺血性脑卒中的认识和预防提供新的临床和实验依据。
方法：本研究包括269例缺血性卒中患者和182例对照组。测量不同疾病阶段的CTRP9和APN多聚体的血清水平。
结果：血清CTRP9，总APN（tAPN），高分子量(HMW)APN在I期(急性期，发病72小时内）缺血性卒中，并在III期（第11天至1个月）和IV期（1个月后）增加，与控制相比。在非高脂血症组中，血清CTRP9,tAPN,与对照组相比，缺血性卒中患者的HMW降低（P<0.05）。血清CTRP9与血清tAPN、HMW密切相关(r=0.992、0.991)。血清CTRP9对缺血性脑卒中具有保护作用(OR=0.400,95%CI0.197~0.810,P<0.05)。
结论：降低血清CTRP9，tAPN，LMW,和HMW与非高脂血症受试者缺血性卒中风险增加显著相关。CTRP9,tAPN,HMW亚型可能是缺血性卒中患者有价值的临床指标。
方法：本研究包括269例缺血性卒中患者和182例对照组。测量不同疾病阶段的CTRP9和APN多聚体的血清水平。
结果：血清CTRP9，总APN（tAPN），高分子量(HMW)APN在I期(急性期，发病72小时内）缺血性卒中，并在III期（第11天至1个月）和IV期（1个月后）增加，与控制相比。在非高脂血症组中，血清CTRP9,tAPN,与对照组相比，缺血性卒中患者的HMW降低（P<0.05）。血清CTRP9与血清tAPN、HMW密切相关(r=0.992、0.991)。血清CTRP9对缺血性脑卒中具有保护作用(OR=0.400,95%CI0.197~0.810,P<0.05)。
结论：降低血清CTRP9，tAPN，LMW,和HMW与非高脂血症受试者缺血性卒中风险增加显著相关。CTRP9,tAPN,HMW亚型可能是缺血性卒中患者有价值的临床指标。
