Tanshinone IIA alleviates blast-induced inflammation, oxidative stress and apoptosis in mice partly by inhibiting the PI3K/Akt/FoxO1 signaling pathway

Liu, Yunen; Tong, Changci; Tang, Yu; Cong, Peifang; Liu, Ying; Shi, Xiuyun; Shi, Lin; Zhao, Yan; Jin, Hongxu; Li, Jing; Hou, Mingxiao

doi:10.1016/j.freeradbiomed.2020.02.032

Cited by 35 publications

(21 citation statements)

References 31 publications

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“…Tanshinone IIA has various activities including cardioprotective, anti-atherosclerotic, anti-cancer, anti-bacterial and anti-viral activities. Moreover, tanshinone IIA increased the survival rate as well as attenuated lung histopathologic changes and lung edema in animals with ALI induced by LPS, paraquat, seawater, bleomycin, pancreatitis or aspiration [ [88] , [89] , [90] , [91] , [92] ]. Interestingly, tanshinone IIA exerted inhibitory effects on lung inflammatory condition via inhibition of expression of pro-inflammatory cytokines TNF-a, IL-1β and IL-6.…”

Section: Natural Compounds That Exert Anti-ali Effectsmentioning

confidence: 99%

“…Additionally, tanshinone IIA could prevent oxidative stress through up-regulating the Nrf2 signaling pathway [ 88 ]. Apoptosis, an important role in ALI, was also suppressed by tanshinone IIA through up-regulating Bcl-2 and down-regulating Bax and Caspase-3, which were partly mediated by the inhibition of the PI3K/Akt/FoxO1 signaling pathway [ 91 ]. At the same time, tanshinone IIA also inhibited lung edema and lung damage via inhibition of AQP1 and AQP5 over-expression [ 96 ].…”

Section: Natural Compounds That Exert Anti-ali Effectsmentioning

confidence: 99%

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Natural product derived phytochemicals in managing acute lung injury by multiple mechanisms

Zhou

et al. 2021

Pharmacological Research

248

121

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Section: Natural Compounds That Exert Anti-ali Effectsmentioning

confidence: 99%

Section: Natural Compounds That Exert Anti-ali Effectsmentioning

confidence: 99%

Natural product derived phytochemicals in managing acute lung injury by multiple mechanisms

Zhou

et al. 2021

Pharmacological Research

248

121

View full text Add to dashboard Cite

show abstract

“…In a hypoxic microenvironment, tanshinone IIA was shown to decrease hypoxia-inducible factor α expression and suppress the secretion of vascular endothelial growth factor and basic fibroblast growth factor by regulating the b-catenin/TCF3/LEF1 signaling pathway, leading to the inhibition of proliferation, tube formation and metastasis of human umbilical vein endothelial cells (6). In addition, tanshinone IIA inhibited PI3K/Akt/FoxO1 signaling and alleviated blast-induced inflammation and oxidative stress, leading to improvement in lung blast injuries (7). Importantly, treatment with tanshinone IIA significantly suppressed proliferation and induced apoptosis in various cancer cell types, including ovarian cancer (8), cervical cancer (9) and gastric cancer (10).…”

Section: Introductionmentioning

confidence: 99%

Tanshinone IIA regulates microRNA‑125b/foxp3/caspase‑1 signaling and inhibits cell viability of nasopharyngeal carcinoma

2021

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Nasopharyngeal carcinoma (NPC) is a common disease with high prevalence worldwide, affecting hundreds of thousands of patients every year. Although its progress can be inhibited by concurrent chemoradiotherapy and platinum-based agents, there is also a need for novel drugs to treat NPC. The present study identified tanshinone IIA as a potent drug that could suppress the proliferation of HK1 cells by enhancing pyroptosis via regulation of the miR-125b/foxp3/caspase-1 signaling pathway. Firstly, the effects of tanshinone IIA on HK1 cells were assessed and it was confirmed that treatment with tanshinone IIA significantly decreased the proliferation of HK1 cells, with increased activity of caspase-3 and caspase-9. Then, the pyroptosis levels after tanshinone IIA administration were detected. The results showed that tanshinone IIA enhanced pyroptosis in a dose-dependent manner. Furthermore, the mechanism underlying the effects of tanshinone IIA on HK1 cells were explored. It was found that transfection with a microRNA (miR)-125b agomir and a small interfering RNA (si)-foxp3 plasmid reversed the inhibitory effect induced by tanshinone IIA, accompanied by an increase in reactive oxygen species levels and lactate dehydrogenase release, indicating a critical role of miR-125b/foxp3 signaling in pyroptosis in HK1 cells. In conclusion, the present study demonstrates that tanshinone IIA enhances pyroptosis and inhibits the proliferation of HK1 cells by modulating miR-125b/foxp3/caspase-1/GSDMD signaling. It is the first study to reveal the inhibitory effect of tanshinone IIA on HK1 cells and to demonstrate the critical role of miR-125b/foxp3 signaling in mediating these effects, providing robust evidence for the treatment of NPC.

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“…Its sodium sulfonate products Sodium Tanshinone Sulfonate A (STS) is the water-soluble modi cation. Because of its anti-in ammatory, antioxidative, and anti-apoptotic pharmacological effects, STS is a widely recognized clinical drug for treating cardiovascular diseases [20][21][22]. Recent researches have shown that STS inhibited collagen deposition in the glomerular basement membrane of diabetic animals by regulating the PERK pathway to alleviate endoplasmic reticulum stress [23], and transcriptome analysis of mesangial cells in animals with diabetic nephropathy showed that STS had a signi cant protective effect on DKD [24].…”

Section: Introductionmentioning

confidence: 99%

STS Protects Diabetic Glomerular Vascular Endothelial Barrier by Ameliorating EPC Dysfunction: Targeting RAGE-TXNIP-NLRP3 Inflammasome Pathway

Heng

Zhang

Wang

et al. 2021

Preprint

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Background: Glomerular endothelial cell (GEC) injury is one of the crucial causes of diabetic kidney disease (DKD). Endothelial progenitor cell (EPC) is the essential mechanism of vascular endothelial repair, which damages by diabetic pathology. Sodium Tanshinone Sulfonate ⅡA (STS) is known to protect endothelium, but the mechanism and the role in DKD need to be studied. Methods: EPC was treated with high glucose (HG), and thioredoxin interacting protein (TXNIP), NLR family pyrin domain containing 3 (NLRP3) inflammasome, DNA damage, proliferation, differentiation and senescence were detected; STS and EPC were intravenous injected into diabetic nude mice, the urine protein quantitation and urine protein/creatinine were detected; the Dil-labeled EPC was traced and the expression of TXNIP, caspase-1 (p20), p21, Ki67, CD31 were detected by fluorescence co-location in glomerulus.Results: We found that STS inhibited HG-induced TXNIP expression and NLRP3 inflammasome activation, catalase (CAT) inactivation, DNA damage, senescence； STS restored EPC proliferation and differentiation functions; advanced glycation end products (AGEs) produced in HG treated EPC supernatant, the receptor of AGE (RAGE) blocking inhibited TXNIP expression and NLRP3 inflammasome activation, which mimicked by STS. STS protected EPC functions in diabetic glomerular and enhanced EPC renal function amelioration. Conclusions: We concluded that STS watched CAT activity to prevent HG-induced EPC DNA damage, proliferation, differentiation dysfunction, accelerated senescence by inhibiting the RAGE-TXNIP-NLRP3 inflammasome-caspase-1 pathway.

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Tanshinone IIA alleviates blast-induced inflammation, oxidative stress and apoptosis in mice partly by inhibiting the PI3K/Akt/FoxO1 signaling pathway

Cited by 35 publications

References 31 publications

Natural product derived phytochemicals in managing acute lung injury by multiple mechanisms

Natural product derived phytochemicals in managing acute lung injury by multiple mechanisms

Tanshinone IIA regulates microRNA‑125b/foxp3/caspase‑1 signaling and inhibits cell viability of nasopharyngeal carcinoma

STS Protects Diabetic Glomerular Vascular Endothelial Barrier by Ameliorating EPC Dysfunction: Targeting RAGE-TXNIP-NLRP3 Inflammasome Pathway

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