After publication of the original manuscript, we found that, in Figure 5G (the iWAT row), the two vehicle tissues were identical. This was caused by a cut–paste error during figure preparation. The original picture, original Figure 5G, and corrected Figure 5G are shown below. We also attached the corrected Figure 5. We apologize for this error and will take necessary steps to avoid such mistakes in the future. Figure 5. In vivo antiobesity effects of 1857. Acute food intake suppression induced by lorcaserin (A) or 1857 (B). Overnight fasting mice (n = 8 each group) were treated with lorcaserin (10 mg/kg), 1857 (30 mg/kg), or vehicle 30 min before feeding. Food intake was measured at indicated time points. (C–G) 1857 inhibited food intake and showed antiobesity effects in a diet-induced obesity (DIO) mouse model. DIO mice (n = 9 each group) were treated with 1857 (30 mg/kg) or vehicle daily for 10 days. Accumulative food intake (C) and body weight change (D) were recorded during the treatment. Blood and liver were collected to measure blood glucose, serum cholesterol (TC), and triglyceride (TG) levels (E) as well as liver TC and TG levels (F). (G) The weight of white adipose tissues (WAT) was also measured, and representative tissue images are shown. Data represent means ± SEM *P < 0.05, **P < 0.01, and ***P < 0.001 (two-tailed Student’s t-test). This article has not yet been cited by other publications. Figure 5. In vivo antiobesity effects of 1857. Acute food intake suppression induced by lorcaserin (A) or 1857 (B). Overnight fasting mice (n = 8 each group) were treated with lorcaserin (10 mg/kg), 1857 (30 mg/kg), or vehicle 30 min before feeding. Food intake was measured at indicated time points. (C–G) 1857 inhibited food intake and showed antiobesity effects in a diet-induced obesity (DIO) mouse model. DIO mice (n = 9 each group) were treated with 1857 (30 mg/kg) or vehicle daily for 10 days. Accumulative food intake (C) and body weight change (D) were recorded during the treatment. Blood and liver were collected to measure blood glucose, serum cholesterol (TC), and triglyceride (TG) levels (E) as well as liver TC and TG levels (F). (G) The weight of white adipose tissues (WAT) was also measured, and representative tissue images are shown. Data represent means ± SEM *P < 0.05, **P < 0.01, and ***P < 0.001 (two-tailed Student’s t-test).

中文翻译：

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对“从筛选草药提取物中发现的G蛋白偶联受体的新型G蛋白偏置和亚型选择性激动剂”的更正。

在原始手稿出版后，我们发现在图5G（iWAT行）中，两个媒介组织是相同的。这是由图形准备过程中的剪切粘贴错误引起的。原始图片，原始图5G和校正后的图5G如下所示。我们还附上​​了更正后的图5。对于此错误，我们深表歉意，并将采取必要的措施以避免将来出现此类错误。图5. 1857年的体内抗肥胖作用。氯西林（A）或1857（B）引起的急性食物摄入抑制。隔夜空腹小鼠（ñ喂食前30分钟，用氯卡色林（10 mg / kg），1857（30 mg / kg）或赋形剂处理（每组= 8）。在指定的时间点测量食物摄入量。（CG）1857在饮食诱导的肥胖症（DIO）小鼠模型中抑制了食物摄入并显示出抗肥胖作用。DIO小鼠（Ñ = 9各组）用1857年处理的每日（30毫克/公斤）或载体10天。治疗期间记​​录了累积食物摄入量（C）和体重变化（D）。收集血液和肝脏以测量血糖，血清胆固醇（TC）和甘油三酸酯（TG）水平（E）以及肝脏TC和TG水平（F）。（G）还测量了白色脂肪组织（WAT）的重量，并显示了代表性的组织图像。数据表示平均值±SEM * P <0.05，** P<0.01，并且*** P <0.001（两尾学生t检验）。本文尚未被其他出版物引用。图5. 1857年的体内抗肥胖作用。氯西林（A）或1857（B）引起的急性食物摄入抑制。隔夜空腹小鼠（每组n = 8）在喂食前30分钟接受氯酪蛋白（10 mg / kg），1857（30 mg / kg）或赋形剂处理。在指定的时间点测量食物摄入量。（CG）1857在饮食诱导的肥胖症（DIO）小鼠模型中抑制了食物摄入并显示出抗肥胖作用。DIO小鼠（ñ每组= 9）每天接受1857（30 mg / kg）或赋形剂治疗10天。治疗期间记​​录了累积食物摄入量（C）和体重变化（D）。收集血液和肝脏以测量血糖，血清胆固醇（TC）和甘油三酸酯（TG）水平（E）以及肝脏TC和TG水平（F）。（G）还测量了白色脂肪组织（WAT）的重量，并显示了代表性的组织图像。数据表示平均值±SEM * P <0.05，** P <0.01和*** P <0.001（两尾学生t检验）。