RETRACTED ARTICLE: Amygdalin reduces lipopolysaccharide-induced chronic liver injury in rats by down-regulating PI3K/AKT, JAK2/STAT3 and NF-κB signalling pathways

Yang, Yang; Zhao, Jie; Song, Xiaolong; Li, Lifeng; Li, Fuqin; Shang, Jia; Wang, Weiwei

doi:10.1080/21691401.2019.1634084

Cited by 25 publications

(18 citation statements)

References 40 publications

(41 reference statements)

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“…It was reported that TREM1 expression in splenic conventional dendritic cells was strongly up-regulated, which subsequently elicited the activation of STAT3 (37). Inhibition of STAT3 signal pathway was also shown to prevent α-synuclein-induced neuroinflammation and LPS-induced chronic liver injury (38,39). Our current study has indicated that the mitochondrial ETC inhibitors can significantly decrease the ratio of p-STAT3 / STAT3 in the LPS-treated BV2 microglia.…”

Section: Discussionsupporting

confidence: 59%

Mitochondrial Electron Transport Chain Inhibition Suppresses LPS-Induced Inflammatory Responses via TREM1/STAT3 Pathway in BV2 Microglia

Zhou

Zhang

Ying

2019

Preprint

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Mitochondrial damage and neuroinflammation belong to two of the most important pathological factors in multiple neurological disorders. However, the effect of mitochondrial damage of microglia on microglial activation under pathological conditions has remained unclear. In our current study, we used BV2 microglia as a cellular model to determine the effects of mitochondrial electron transport chain (ETC) inhibitors on LPS-induced inflammatory responses of microglia. We found that all of the three mitochondrial ETC inhibitors, including rotenone, sodium azide and antimycin A, significantly inhibited LPS-induced inflammatory responses of the microglia, assessed by determinations of the protein or mRNA levels of IL-1, IL-6, TNF- iNOS and COX2Nuclear translocation of NF-B p65 subunit does not appear to play an important role in the mitochondrial ETC inhibition-produced suppression of microglial activation. Instead, our study found that the mitochondrial ETC inhibitors significantly attenuated not only the LPS-induced increase in the TREM1 levels -an amplifier of inflammatory process, but also the LPS-induced increase in the ratio of phosphorylated STAT3 / STAT3. In summary, our study has suggested that mitochondrial ETC inhibition of microglia can lead to suppression of LPS-induced microglial activation, which may be mediated by the inhibitory effects of mitochondrial ETC inhibition on the LPS-induced increases in the level of TREM1 and the ratio of p-STAT3 / STAT3. These findings have provided valuable information for elucidating the relationships between mitochondrial damage and neuroinflammation in multiple neurological diseases.

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Section: Discussionsupporting

confidence: 59%

Mitochondrial Electron Transport Chain Inhibition Suppresses LPS-Induced Inflammatory Responses via TREM1/STAT3 Pathway in BV2 Microglia

Zhou

Zhang

Ying

2019

Preprint

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“…Numerous studies have supported that amygdalin can induce apoptotic cell death of various cancer cells such as promyelocytic leukemia, prostate cancer, liver cancer, and cervical cells . Also, amygdalin has various activities including inhibition of fibrosis, anticancer, anti‐inflammation, anti‐ulcer activities and inhibition of kidney interstitial fibrosis, resistance to hyperoxia‐induced lung injury and prevention of pulmonary fibrosis .…”

Section: Introductionmentioning

confidence: 99%

“…22,23,[28][29][30][31] Numerous studies have supported that amygdalin can induce apoptotic cell death of various cancer cells such as promyelocytic leukemia, prostate cancer, liver cancer, and cervical cells. 25,[32][33][34] Also, amygdalin has various activities including inhibition of fibrosis, anticancer, anti-inflammation, anti-ulcer activities and inhibition of kidney interstitial fibrosis, resistance to hyperoxia-induced lung injury and prevention of pulmonary fibrosis. 22,23,27,31,32,35,36 Therefore, the current study aimed to shows the renal ameliorative role of VB17 against EAC induced kidney toxicity, injury, DNA damage, proliferation, and apoptosis alterations.…”

mentioning

confidence: 99%

Ameliorative effects of vitamin B17 on the kidney against Ehrlich ascites carcinoma induced renal toxicity in mice

Mutar

Tousson

Hafez

et al. 2019

Environmental Toxicology

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Cancer is the major cause of death and many factors that lead to its occurrences, such as environmental pollution and pesticides and other factors. Ehrlich carcinoma development depends on many things associated with the environment, nutrition, personal habits, and family history. The present study aimed to evaluate the potential protective effects of vitamin B17 (VB17) against Ehrlich ascites carcinoma (EAC) that induced kidney toxicity in female mice. The mice were divided into five groups (first group, control group; second group, VB17 group; third group, EAC group; fourth group, pretreated EAC with VB17; fifth group, cotreated EAC with VB17). Results showed the VB17 in pretreated (G4) and cotreated (G5) groups lead to an improvement in DNA damage and cytological examination, in addition significantly (P < .05) increase in Na+, red blood cell, hemoglobin, hematocrit value, mean corpuscular hemoglobin (MCH), and MCH concentration, whereas significantly (P < .05) decrease in urea, creatinine, K+, platelets, and white blood cells while insignificant (P < .05) changes in mean corpuscular volume when compared to the EAC group. Many histopathological changes were observed in kidney sections in EAC as marked damage and degenerated, glomerular atrophy, the Malpighian corpuscles that lost their characteristic configuration. On the other hand, a moderate improvement and arrangement in the kidney histological structure in pretreated VB17 + EAC, while a mild enhancement and arrangement of the kidney structure in cotreated EAC + VB17. In addition, depletion in renal P53 and PCNA protein expression compared with the EAC group. It could be concluded that VB17 has a potential renal protective effect against EAC cells induced kidney injury.

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“…It has been reported that STAT3, which mediates type I interferon signaling, is associated with inflammation. There is also evidence that inhibition of JAK2/STAT3 signal pathway might help prevent LPS-induced inflammation 32,33. Besides, inhibitors of the JAK2/STAT3 pathway have been shown to significantly ameliorate HG/AngII-induced inflammation 34,35.…”

Section: Resultsmentioning

confidence: 99%

<p>Luteolin Attenuates Atherosclerosis Via Modulating Signal Transducer And Activator Of Transcription 3-Mediated Inflammatory Response</p>

Ding¹,

Zheng²,

Yang³

et al. 2019

DDDT

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BackgroundInflammatory factors play a crucial role throughout the development and progression of atherosclerosis, which has been considered as a chronic vascular inflammatory disease. Luteolin, a natural flavonoid which exists in many natural medicinal materials, has anti-inflammatory, anti-fibrotic and other pharmacological effects. Recently, the protective effects of luteolin on the cardiovascular disease have been reported. However, there is a paucity of studies on anti-atherosclerosis. Therefore, the anti-atherosclerosis potential of luteolin remains to be elucidated.MethodApoE-/- mice were fed with a high-fat diet to induce atherosclerosis in an animal model, where they were treated with oral administration of luteolin for 12 weeks. Primary mouse peritoneal macrophages challenged with oxidized low-density lipoprotein (oxLDL) were used for in vitro mechanistic study. The effectiveness of luteolin in the ApoE-/- mouse model of atherosclerosis was estimated in the aortic sinus and enface, and the underlying mechanisms were explored by molecular modeling study and siRNA-induced gene silencing.ResultsOur results showed that luteolin remarkably attenuated atherosclerosis in high-fat diet-induced ApoE-/- mouse via alleviating inflammation. We further found that luteolin decreased oxLDL-induced inflammation by inhibiting signal transducer and activator of transcription 3 (STAT3) in vitro, respectively. Further molecular modeling analysis indicated that luteolin interacted with STAT3 primarily through hydrogen bond interaction.ConclusionLuteolin could be a promising candidate molecule for atherosclerosis, and STAT3 may be a potential therapeutic target that could prevent the development of atherosclerosis.

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RETRACTED ARTICLE: Amygdalin reduces lipopolysaccharide-induced chronic liver injury in rats by down-regulating PI3K/AKT, JAK2/STAT3 and NF-κB signalling pathways

Abstract: Wang (2019) Amygdalin reduces lipopolysaccharide-induced chronic liver injury in rats by downregulating PI3K/AKT, JAK2/STAT3 and NF-κB signalling pathways,

Cited by 25 publications

References 40 publications

Mitochondrial Electron Transport Chain Inhibition Suppresses LPS-Induced Inflammatory Responses via TREM1/STAT3 Pathway in BV2 Microglia

Mitochondrial Electron Transport Chain Inhibition Suppresses LPS-Induced Inflammatory Responses via TREM1/STAT3 Pathway in BV2 Microglia

Ameliorative effects of vitamin B17 on the kidney against Ehrlich ascites carcinoma induced renal toxicity in mice

<p>Luteolin Attenuates Atherosclerosis Via Modulating Signal Transducer And Activator Of Transcription 3-Mediated Inflammatory Response</p>

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