Schisandrin B Prevents Hind Limb from Ischemia-Reperfusion-Induced Oxidative Stress and Inflammation via MAPK/NF-<i>κ</i>B Pathways in Rats

Zhu, Ning; Cai, Changhong; Zhou, Aiming; Zhao, Xuyong; Xiang, Yijia; Zeng, Chunlai

doi:10.1155/2017/4237973

Cited by 30 publications

(22 citation statements)

References 35 publications

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“…Evodiamine inhibited IκBα phosphorylation to inactivate NF-κB expression to relieve zymosan-induced inflammation ( Fan et al., 2017 ). Schisandrin B or psoralen ameliorated chondrocyte inflammation and osteoarthritis, oxidative stress injury, and DSS-induced colitis via suppression of the NF-κB/MAPK signaling pathways, followed by decreased inflammatory cytokines ( Liu et al., 2015a , b ; Li et al., 2017 ; Zhu et al., 2017 ; Ran et al., 2018 ). We have previously found that SSW inhibited P38 MAPK mRNA expression to downregulate colonic epithelial cell apoptosis in colonic mucosa in mice with colitis ( Zhao et al., 2013 ).…”

Section: Discussionmentioning

confidence: 99%

Sishen Wan® Ameliorated Trinitrobenzene-Sulfonic-Acid-Induced Chronic Colitis via NEMO/NLK Signaling Pathway

et al. 2019

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The nuclear factor (NF)-κB signaling pathway plays an important role in the initialization and development phase of inflammatory injuries, including inflammatory bowel disease (IBD). Sishen Wan (SSW) is a classic Chinese patent medicine listed in the Chinese Pharmacopoeia, which is usually used to treat chronic colitis; however, it is unclear whether SSW can treat IBD via the NF-κB signaling pathway. In the present study, the therapeutic effect of SSW was demonstrated by the decreased index of colonic weight, macroscopic and microscopic score, and pathological observation in chronic colitis induced by trinitrobenzene sulfonic acid. In colonic mucosa of rats with chronic colitis, SSW reduced the levels of calprotectin and eliminated oxidative lesions; downregulated expression of interferon-γ, interleukin (IL)-1β and IL-17; increased expression of IL-4; and suppressed expression of NF-κB p65, and NF-κB essential modulator (NEMO)-like kinase (NLK). Furthermore, SSW inhibited ubiquitinated NEMO, ubiquitin-activated enzyme, and E2i activation, and phosphorylation of downstream proteins (cylindromatosis protein, transforming growth factor-β-activated kinase and P38). These results show that the therapeutic effects of SSW in chronic colitis were mediated by inhibiting the NEMO/NLK signaling pathway to suppress NF-κB activation.

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Section: Discussionmentioning

confidence: 99%

Sishen Wan® Ameliorated Trinitrobenzene-Sulfonic-Acid-Induced Chronic Colitis via NEMO/NLK Signaling Pathway

et al. 2019

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“…And it belongs to dibenzocyclooctadiene derivatives chemically. In general, Schisandrin B has shown various benefits in different organs and diseases, such as osteoarthritis, renal fibrosis, and myocardial ischemia ( Ran et al, 2018 ; Zhao et al, 2018 ; Cao et al, 2019 ), and it has been reported to regulate several signaling pathways, including NF-κB, MAPK, PI3K/AKT, and Nrf2/HO-1 pathways ( Zhu et al, 2017 ; Feng et al, 2018 ; Zhao et al, 2018 ; You et al, 2019 ).…”

Section: Discussionmentioning

confidence: 99%

Schisandrin B Inhibits Osteoclastogenesis and Protects Against Ovariectomy-Induced Bone Loss

et al. 2020

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Osteoporosis is a systemic skeletal disease which is highly prevalent worldwide and considered to be associated with excessive bone resorption mediated by osteoclast. Osteoclast differentiation is featured by the activation of inflammation-related pathways and the generation of reactive oxygen species. Schisandrin B is a bioactive compound with strong antiinflammation and antioxidative properties, we thus speculated that Schisandrin B might serve as a potential candidate for osteoporosis. In the present study, we found that the formation and` function of osteoclasts were dramatically suppressed by Schisandrin B. And consistent with the in vitro results, treatment with Schisandrin B attenuated ovariectomy-induced bone loss in mice. Moreover, Schisandrin B notably inhibited the activation of mitogen activated protein kinase (MAPK) and nuclear factor-κB (NF-κB) pathways and scavenged ROS by activating nuclear factor E2 p45-related factor 2 (Nrf2) signaling. In conclusion, our study indicates that Schisandrin B is an effective approach to treat osteoporosis and other osteoclast-related diseases.

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“…It is well known that MAPKs (p38, ERK, and JNK) signaling pathways are highly associated with oxidative stress-induced cell death ( 41 - 43 ). Other studies have shown that overexpression of IDO-1 protein inhibited the activation of Akt and MAPKs signaling pathways and regulated apoptotic protein expression levels in neuronal cells under excessive oxidative stress ( 44 , 45 ).…”

Section: Discussionmentioning

confidence: 99%

Tat-indoleamine 2,3-dioxygenase 1 elicits neuroprotective effects on ischemic injury

et al. 2020

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It is well known that oxidative stress participates in neuronal cell death caused production of reactive oxygen species (ROS). The increased ROS is a major contributor to the development of ischemic injury. Indoleamine 2,3-dioxygenase 1 (IDO-1) is involved in the kynurenine pathway in tryptophan metabolism and plays a role as an anti-oxidant. However, whether IDO-1 would inhibit hippocampal cell death is poorly known. Therefore, we explored the effects of cell permeable Tat-IDO-1 protein against oxidative stress-induced HT-22 cells and in a cerebral ischemia/reperfusion injury model. Transduced Tat-IDO-1 reduced cell death, ROS production, and DNA fragmentation and inhibited mitogen-activated protein kinases (MAPKs) activation in H2O2 exposed HT-22 cells. In the cerebral ischemia/ reperfusion injury model, Tat-IDO-1 transduced into the brain and passing by means of the blood-brain barrier (BBB) significantly prevented hippocampal neuronal cell death. These results suggest that Tat-IDO-1 may present an alternative strategy to improve from the ischemic injury. [BMB Reports 2020; 53(11): 582-587]

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Schisandrin B Prevents Hind Limb from Ischemia-Reperfusion-Induced Oxidative Stress and Inflammation via MAPK/NF-κB Pathways in Rats

Cited by 30 publications

References 35 publications

Sishen Wan® Ameliorated Trinitrobenzene-Sulfonic-Acid-Induced Chronic Colitis via NEMO/NLK Signaling Pathway

Sishen Wan® Ameliorated Trinitrobenzene-Sulfonic-Acid-Induced Chronic Colitis via NEMO/NLK Signaling Pathway

Schisandrin B Inhibits Osteoclastogenesis and Protects Against Ovariectomy-Induced Bone Loss

Tat-indoleamine 2,3-dioxygenase 1 elicits neuroprotective effects on ischemic injury

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