Corrigendum to “Anti-TNF-α monoclonal antibody reverses psoriasis through dual inhibition of inflammation and angiogenesis” [Int. Immunopharmacol. 28(1) (2015) 731–743]

Liu, Yu; Yang, Guoyou; Zhang, Junfeng; Xing, Kaiyan; Dai, Lei; Cheng, Lin; Deng, Jie; Shi, Gang; Li, Chunlei; Su, Xiaolan; Zhang, Shuang; Yang, Yang; Li, Jia; Yu, Dechao; Xiang, Rong; Wei, Yuquan; Deng, Hongxin

doi:10.1016/j.intimp.2020.107019

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“…[ 13 ] However, the relapsing nature of the disease and serious side effects like hypersensitivity reactions, dyspepsia, hepato‐nephrotoxicity, and drug dependence serve as a reminder of the necessity for a strong complementary and alternative therapy against UC. [ 14 ] Biochanin A (5,7‐dihydroxy‐4′‐methoxy‐isoflavone) is a phytoestrogen derived from plants such as red clover, cabbage, and alfalfa. It has a wide spectrum of medicinal value, including anti‐inflammatory and antioxidant, [ 15,16 ] anticarcinogenic, [ 17 ] neuroprotective, [ 18 ] and antihyperglycemic [ 19 ] activities.…”

Section: Introductionmentioning

confidence: 99%

Biochanin A mitigates ulcerative colitis and intestinal inflammation in mice by inhibiting MAPK/NF‐kB (p65) axis

Kulhari,

Rajanan,

Ambujakshan

et al. 2024

J Biochem & Molecular Tox

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Ulcerative colitis (UC) is a chronic problem of the intestine and relapsing in nature. Biochanin A is a nature‐derived isoflavonoid and has numerous bioactivities. However, its role against UC and intestinal inflammation remains obscure. We aimed to comprehensively explore the pharmacological effect of biochanin A in alleviating colitis and to evaluate the potential mechanisms. Initially, we explored the anti‐inflammatory action of biochanin A (15, 30, and 60 μM) by employing lipopolysaccharide (LPS)‐activated RAW 264.7 cells. In RAW 264.7 cells under LPS stimulation, biochanin A inhibited the elevation of reactive oxygen species (ROS) (p < 0.0001), interleukin (IL)−1β (p < 0.0001), IL‐18 (p < 0.01), and tumor necrosis factor (TNF)‐α (p < 0.01) release, nitrite production (p < 0.0001), and the expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase‐2 (COX‐2) proteins. Next, we studied the effectiveness of biochanin A (20 and 40 mg/kg) in mouse colitis induced with dextran sulfate sodium (DSS) by assessing colon length, disease activity index (DAI) scoring, and performing colonoscopy and histological analysis. The pro‐inflammatory cytokines were estimated using ELISA. Western blot studies were performed to assess underlying mechanisms. In mice, biochanin A treatment alleviated DAI score (p < 0.0001), restored colon length (p < 0.05) and morphology, and re‐established colon histopathology. Biochanin A affects the phosphorylation of proteins associated with NF‐κB (p65) and mitogen‐activated protein kinase (MAPK) axis and regulates colonic inflammation by reducing the expression of inflammatory cytokines and myeloperoxidase (MPO) activity. Altogether, our findings support the idea that the anticolitis potential of biochanin A is allied with anti‐inflammatory activity by inhibiting the MAPK/NF‐κB (p65) axis. Hence, biochanin A may be an alternative option to alleviate the risk of colitis.

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