Radiation Biology and Health Sciences Division, Bhabha Atomic Research Centre, Trombay, Mumbai 400085, India.
J Biosci. 2023;48(2). doi: 10.1007/s12038-023-00329-3.
The present study primarily focuses on the efficacy of Malabaricone C (Mal C) as an anti-inflammatory agent. Mal C inhibited mitogen-induced T-cell proliferation and cytokine secretion. Mal C significantly reduced cellular thiols in lymphocytes. -acetyl cysteine (NAC) restored cellular thiol levels and abrogated Mal C-mediated inhibition of T-cell proliferation and cytokine secretion. Physical interaction between Mal C and NAC was evinced from HPLC and spectral analysis. Mal C treatment significantly inhibited concanavalin A-induced phosphorylation of ERK/JNK and DNA binding of NF-κB. Administration of Mal C to mice suppressed T-cell proliferation and effector functions . Mal C treatment did not alter the homeostatic proliferation of T-cells but completely abrogated acute graft-versus-host disease (GvHD)-associated morbidity and mortality. Our studies indicate probable use of Mal C for prophylaxis and treatment of immunological disorders caused due to hyper-activation of T-cells.
本研究主要关注马拉巴酮 C(Mal C)作为一种抗炎剂的功效。Mal C 抑制有丝分裂原诱导的 T 细胞增殖和细胞因子分泌。Mal C 可显著降低淋巴细胞中的细胞硫醇。N-乙酰半胱氨酸(NAC)可恢复细胞硫醇水平,并消除 Mal C 介导的 T 细胞增殖和细胞因子分泌抑制作用。从 HPLC 和光谱分析中证实了 Mal C 和 NAC 之间的物理相互作用。Mal C 处理显著抑制刀豆蛋白 A 诱导的 ERK/JNK 磷酸化和 NF-κB 的 DNA 结合。给予 Mal C 可抑制小鼠 T 细胞增殖和效应功能。Mal C 处理不会改变 T 细胞的稳态增殖,但完全消除了急性移植物抗宿主病(GvHD)相关的发病率和死亡率。我们的研究表明,Mal C 可能用于预防和治疗由于 T 细胞过度激活引起的免疫性疾病。