Medicherla Kanakaraju, Ketkar Avanee, Sahu Bidya Dhar, Sudhakar Godi, Sistla Ramakrishna
Department of Human Genetics, College of Science and Technology, Andhra University, Visakhapatnam 530003, India.
Medicinal Chemistry and Pharmacology Division, CSIR-Indian Institute of Chemical Technology (IICT), Hyderabad 500 007, India.
Food Funct. 2016 Jul 13;7(7):3233-43. doi: 10.1039/c6fo00244g.
We investigated the anti-inflammatory and anti-colitis effects of Rosmarinus officinalis L. extract (RE) by using both in vitro LPS-activated mouse RAW 264.7 macrophages and in vivo dextran sulfate sodium (DSS)-induced experimental murine colitis and suggested the underlying possible mechanisms. Liquid Chromatography-Mass Spectrometry (LC-MS) analysis was performed to identify the major components present in the RE. The clinical signs, biochemistry, immunoblot, ELISA and histology in colon tissues were assessed in order to elucidate the beneficial effect of RE. RE suppressed the LPS-induced pro-inflammatory cytokine production and the expressions of inflammatory proteins in macrophages. Administration of RE (50 and 100 mg kg(-1)) also significantly reduced the severity of DSS-induced murine colitis, as assessed by the clinical symptoms, colon length and histology. RE administration prevented the DSS-induced activation of p38, ERK and JNK MAPKs, attenuated IκBα phosphorylation and subsequent nuclear translocation and DNA binding of NF-κB (p65). RE also suppressed the COX-2 and iNOS expressions, decreased the levels of TNF-α and IL-6 cytokines and the myeloperoxidase activity in the colon tissue. Histological observation revealed that RE administration alleviated mucosal damage and inflammatory cell infiltration induced by DSS in the colon tissue. Hence, RE could be used as a new preventive and therapeutic food ingredient or as a dietary supplement for inflammatory bowel disease.
我们通过体外脂多糖(LPS)激活的小鼠RAW 264.7巨噬细胞和体内葡聚糖硫酸钠(DSS)诱导的实验性小鼠结肠炎,研究了迷迭香叶提取物(RE)的抗炎和抗结肠炎作用,并提出了潜在的可能机制。采用液相色谱-质谱联用(LC-MS)分析来鉴定RE中的主要成分。评估结肠组织的临床症状、生化指标、免疫印迹、酶联免疫吸附测定(ELISA)和组织学,以阐明RE的有益作用。RE抑制了LPS诱导的巨噬细胞中促炎细胞因子的产生以及炎症蛋白的表达。给予RE(50和100 mg kg⁻¹)也显著降低了DSS诱导的小鼠结肠炎的严重程度,这通过临床症状、结肠长度和组织学评估得出。给予RE可防止DSS诱导的p38、细胞外信号调节激酶(ERK)和c-Jun氨基末端激酶(JNK)丝裂原活化蛋白激酶(MAPKs)的激活,减弱IκBα磷酸化以及随后核因子κB(NF-κB,p65)的核转位和DNA结合。RE还抑制了环氧化酶-2(COX-2)和诱导型一氧化氮合酶(iNOS)的表达,降低了结肠组织中肿瘤坏死因子-α(TNF-α)和白细胞介素-6(IL-6)细胞因子的水平以及髓过氧化物酶活性。组织学观察显示,给予RE可减轻DSS诱导的结肠组织黏膜损伤和炎症细胞浸润。因此,RE可作为一种新的预防和治疗食品成分或作为炎症性肠病的膳食补充剂。