Baicalein inhibits TNF-α-induced NF-κB activation and expression of NF-κB-regulated target gene products

Li, Junbo; Ma, Juan; Wang, Ke Si; Mi, Chunliu; Wang, Zhe; Piao, Lian Xun; Xu, Guang; Li, Xuezheng; Lee, Jun Young; Jin, Xuejun

doi:10.3892/or.2016.5108

Cited by 49 publications

(36 citation statements)

References 20 publications

(18 reference statements)

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“…Some inflammatory cytokines could activate I-κBα, and then p65 protein separates from I-κBα and translocates from cytoplasm to the nucleus to bind related inflammation genes to induce inflammation [18]. Many studies provide evidence for the role of NF-κB in mediating enhancement of apoptosis [14,15]. Apoptosis, or programmed cell death, has been suggested to have a close relationship with OA progression [29,30].…”

Section: Discussionmentioning

confidence: 99%

“…Nuclear factor κB (NF-κB) has been considered as a central mediator in diverse cellular responses, particularly in the inflammatory process and immune response [9]. Many studies reported that IL-1β and TNF-α induced the nuclear translocation of NF-κB [10][11][12][13][14]. en, NF-κB activated the downstream Bcl-2 family proteins to regulate apoptosis [15,16].…”

Section: Introductionmentioning

confidence: 99%

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Protective Effect of Genistein on Condylar Cartilage through Downregulating NF-κB Expression in Experimentally Created Osteoarthritis Rats

Jian

Ding

et al. 2019

BioMed Research International

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Temporomandibular joint osteoarthrosis (TMJOA) is characterised by chronic inflammatory changes, with subsequent gradual loss of joint cartilage. NF-κB is a crucial transcription factor in the course of inflammatory and immune responses, which are involved in OA pathology activated by proinflammatory cytokines. Genistein is known to have anti-inflammation and modulation of metabolic pathways through repression of the NF-κB signaling pathway in inflammatory disease. But so far, studies on the effects of genistein on TMJOA are very limited. So, the purpose of this study is to investigate the protective effect of genistein against experimentally induced condylar cartilage degradation through downregulating NF-κB expression in created osteoarthritis rats in vivo. Male SD rats were created as temporomandibular joint osteoarthritis models and administered through oral gavage with low and high dosage genistein (30 mg/kg and 180 mg/kg, respectively) daily for 4 weeks. The morphological changes of the condylar cartilage were studied with HE and Masson staining. The expressions of p65 and inflammatory cytokines (IL-1β and TNFα) were detected using immunohistochemistry and real-time PCR. The results showed that experimentally created osteoarthritis reduced the condylar cartilage thickness of rats and increased the gene expression of cytokines (IL-1β and TNFα) and positive cells of p65. Genistein treatment had positive effects on the condylar cartilage renovation, while high dose genistein treatment had more significant effects on the reversing of OA changes and reduction of the expression of p65 and inflammatory cytokines (IL-1β and TNFα). The results indicated that high dose genistein treatment had obvious therapeutic effects on condyle cartilage damages of OA rats. The mechanism may be that genistein suppresses the NF-κB expression activated by inflammatory cytokines.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Protective Effect of Genistein on Condylar Cartilage through Downregulating NF-κB Expression in Experimentally Created Osteoarthritis Rats

Jian

Ding

et al. 2019

BioMed Research International

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“…One possible mechanism that would potentially explain both the apoptotic and protective effects is the inhibitory action of NF-κB and its-regulated gene expression by Baicalein. Baicalein induced apoptosis in cancer cells by suppression of anti-apoptotic Bcl-2 family proteins via the inhibition of NF-κB (Li et al, 2016). Meanwhile, Baicalein exhibited protective effects mediated by the suppression of iNOS via NF-κB inhibition (Suk et al, 2003).…”

Section: Discussionmentioning

confidence: 99%

The flavonoid Baicalein attenuates cuprizone-induced demyelination via suppression of neuroinflammation

Hashimoto

Yamamoto

Iwasa

et al. 2017

Brain Research Bulletin

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Multiple sclerosis (MS) is a chronic demyelinating disease of the central nervous system characterized by recurrent and progressive demyelination/remyelination cycles, neuroinflammation, oligodendrocyte loss, and axonal pathology. Baicalein isolated from the roots of Scutellaria baicalensis has been shown to exert anti-inflammatory and antioxidant effects. The cuprizone model is an established mouse model of MS and causes demyelination and motor dysfunction and induces neuroinflammation, such as glial activation and pro-inflammatory cytokine production. To determine whether Baicalein attenuates cuprizone-induced demyelination, we administrated Baicalein to cuprizone-exposed mice. Baicalein attenuated weight loss (P<0.05) and motor dysfunction (P<0.05) in the cuprizone model mice. Baicalein treatment effectively suppressed the demyelination (P<0.01) and gene expressions of CNP (P<0.05) and MBP (P<0.05). Baicalein treatment also inhibited the cuprizone-induced increase in Iba1-positive microglia (P<0.001), GFAP-positive astrocytes (P<0.001), and the gene expressions of CD11b (P<0.01), GFAP (P<0.05), TNFα (P<0.05), IL-1β (P<0.05), and iNOS (p<0.01). We found that Baicalein treatment attenuated cuprizone-induced demyelination, glial activation, pro-inflammatory cytokine expression, and motor dysfunction. Our results suggest that Baicalein may be a useful therapeutic agent in demyelinating diseases to suppress neuroinflammation.

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“…[53][54] Not only esculin but also gingerol, baicalein, and wogonin, another active compound interacted with baicelein, have interaction with MMP9 and TNF-α and moreover, some studies have been approved these compounds' effect toward MMP9 and TNF-α. [55][56][57] In tuberculosis treatment, it may be suggested that esculin, gingerol, wogonin, and baicelin reduce the level of TNF-α and MMP9. Furthermore, zingerone found in Zingiber officinallis Rosc also have interaction with TNF-α through catalase.…”

Section: Plants Used For Treating Tuberculosis In Indonesia Provincesmentioning

confidence: 99%

Network Analysis of Indigenous Indonesia Medical Plants for Treating Tuberculosis

Aristyani¹,

Widyarti²,

Sumitro³

2018

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Background: Indonesia is the biggest archipelago country with the second biggest biodiversity in the world. A lot of medical plants for treating various diseases can be found in Indonesia, including medical plants for tuberculosis, an infectious disease caused by Mycobacterium tuberculosis. Objective: The goal of this research is to document the information of Indonesia indigenous medical plants that used various local societies to treat tuberculosis and also analyze active compounds of medical plants with proteins that related to tuberculosis. Methods and Materials: The annotation of medical plants for treating tuberculosis was collected from a various source comprising local research papers, theses, and other resources. The information of active compound was taken from Dr. Duke's Phytochemical and Ethnobotanical Databases. A network of active compounds-proteins was analyzed by using Cytoscape 3.6.0. Results: The result described that there were twenty-seven species from nineteen families of medical plants used by local societies of Indonesia for tuberculosis therapy, and there were sundry of active compounds from fourteen medical plants had direct interaction with proteins related tuberculosis. Conclusion: Most of the active compounds targeted proteins that had a prominent role in immune system. It indicated that medical plants treating tuberculosis through regulating immunity of human body. ABSTRACT SUMMARY • Tuberculosis is a respiratory infectious disease caused by Mycobacterium tuberculosis. For a long time, Indonesia local societies have been used medical plants for tuberculosis therapy. By using network analysis study, the active compounds of medical plants can modulate human immunity to treat tuberculosis. Sherry Aristyani, a master student of Biology in Faculty of Mathematics and Natural Sciences, University of Brawijaya. Her master research focuses on active compounds of Indonesia medical plants for tuberculosis therapy. Sri Widyarti, Lecturer and researcher in Faculty of Mathematics and Natural Sciences, University of Brawijaya. She has expertise in biology cell. Sutiman Bambang Sumitro, a professor in Department of Biology, Faculty of Mathematics and Natural Sciences, University of Brawijaya. He has expertise in biology cell, bioinorganic, and nano-biology. ABOUT AUTHORS

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Baicalein inhibits TNF-α-induced NF-κB activation and expression of NF-κB-regulated target gene products

Cited by 49 publications

References 20 publications

Protective Effect of Genistein on Condylar Cartilage through Downregulating NF-κB Expression in Experimentally Created Osteoarthritis Rats

Protective Effect of Genistein on Condylar Cartilage through Downregulating NF-κB Expression in Experimentally Created Osteoarthritis Rats

The flavonoid Baicalein attenuates cuprizone-induced demyelination via suppression of neuroinflammation

Network Analysis of Indigenous Indonesia Medical Plants for Treating Tuberculosis

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