Rutgers Robert Wood Johnson Medical School, Gout Center and Division of Rheumatology, Department of Medicine, Rutgers Robert Wood Johnson Medical School, New Brunswick, NJ, USA.
AMPEL BioSolutions, Charlottesville, VA, USA.
Clin Exp Rheumatol. 2022 Jul;40(7):1293-1298. doi: 10.55563/clinexprheumatol/xnb7hp. Epub 2021 Jul 24.
To identify the anthocyanin content in tart cherry juice concentrate (TCJC) and establish the anti-inflammatory effect of in a murine acute gout model.
The main anthocyanins in the TCJC were identified by liquid chromatography mass spectroscopy (LCMS). TCJC or phosphate-buffered saline (PBS) as control were administered daily by oral gavage to BALB/C-Tg(NFκB-RE-luc)-Xen mice that harbour a firefly luciferase cDNA reporter under the regulation of 3 Nuclear factor-κB (NF-κB) response elements. After 14 days, gouty inflammation was induced by intra-articular injection of monosodium urate (MSU) crystals into the tibio-tarsal joint (ankle). NF-κB activity was measured locally in the injected ankle using the Xenogen in vivo imaging system (IVIS), and decalcified feet/ankles were paraffin-embedded and analysed histopathologically.
The major anthocyanin compound present in TCJC was cyanidin 3-glucosylrutinoside followed by cyanidin 3-rutinoside. In the murine acute gout model, MSU injection increased NF-κB activity and oral administration of TCJC significantly reduced NF-κB activity in mouse foot, and ankle joints as assessed by IVIS analysis. Bioluminescent imaging detection of NF-κB activation was inhibited approximately 2-fold relative to control mice receiving PBS. Histopathologic examination showed suppression of infiltrates into the tibio-tarsal joint space of the mice receiving TCJC compared to PBS-treated control counterparts.
The major anthocyanin in TCJC was cyanidin 3-glucosylrutinoside. Clinically relevant doses of TCJC significantly inhibit inflammation and NF-κB activation induced by MSU crystals.
鉴定酸樱桃浓缩汁(TCJC)中的花色苷含量,并在小鼠急性痛风模型中确定其抗炎作用。
采用液相色谱-质谱联用(LCMS)鉴定 TCJC 中的主要花色苷。通过口服灌胃,每天给予 BALB/C-Tg(NFκB-RE-luc)-Xen 小鼠 TCJC 或磷酸盐缓冲盐水(PBS)作为对照,该小鼠在 3 个核因子-κB(NF-κB)反应元件的调控下携带萤火虫荧光素酶 cDNA 报告基因。14 天后,通过向跖跗关节(踝关节)内注射单钠尿酸盐(MSU)晶体诱导痛风性炎症。使用 Xenogen 活体成像系统(IVIS)在注射的踝关节局部测量 NF-κB 活性,并对脱钙的脚/踝关节进行石蜡包埋和组织病理学分析。
TCJC 中存在的主要花色苷化合物是矢车菊素 3-葡萄糖基芸香糖苷,其次是矢车菊素 3-鼠李糖苷。在小鼠急性痛风模型中,MSU 注射增加了 NF-κB 活性,而 TCJC 的口服给药显著降低了小鼠足部和踝关节的 NF-κB 活性,通过 IVIS 分析评估。与接受 PBS 的对照小鼠相比,生物发光成像检测到 NF-κB 激活的抑制约为 2 倍。组织病理学检查显示,与接受 PBS 治疗的对照组相比,接受 TCJC 治疗的小鼠胫骨关节间隙的浸润得到抑制。
TCJC 中的主要花色苷为矢车菊素 3-葡萄糖基芸香糖苷。TCJC 的临床相关剂量可显著抑制 MSU 晶体诱导的炎症和 NF-κB 激活。