Cryptotanshinone ameliorates renal ischaemia–reperfusion injury by inhibiting apoptosis and inflammatory response

Bai, Tao; Yang, Kang; Qin, Cong; Xu, Tao; Yu, Xi; Zhang, Jie

doi:10.1111/bcpt.13275

Cited by 16 publications

(6 citation statements)

References 42 publications

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“…Among them, plant derived‐natural compounds are suggested to be beneficial in cancer therapy. A variety of factors contribute to the popularity of naturally occurring compounds in cancer therapy such as multi‐targeting, minimal side effects and low cost (Bai et al, 2019; Banik et al, 2020). These anti‐tumor drugs are abundant in nature and using them in cancer therapy can shed some light on their therapeutic effect to direct further studies in improving their anti‐tumor activity (Kashyap et al, 2019; Lee et al, 2019).…”

Section: Introductionmentioning

confidence: 99%

Recent advances and future directions in anti‐tumor activity of cryptotanshinone: A mechanistic review

Ashrafizadeh

Zarrabi

Orouei

et al. 2020

Phytotherapy Research

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In respect to the enhanced incidence rate of cancer worldwide, studies have focused on cancer therapy using novel strategies. Chemotherapy is a common strategy in cancer therapy, but its adverse effects and chemoresistance have limited its efficacy. So, attempts have been directed towards minimally invasive cancer therapy using plant derived‐natural compounds. Cryptotanshinone (CT) is a component of salvia miltiorrihiza Bunge, well‐known as Danshen and has a variety of therapeutic and biological activities such as antioxidant, anti‐inflammatory, anti‐diabetic and neuroprotective. Recently, studies have focused on anti‐tumor activity of CT against different cancers. Notably, this herbal compound is efficient in cancer therapy by targeting various molecular signaling pathways. In the present review, we mechanistically describe the anti‐tumor activity of CT with an emphasis on molecular signaling pathways. Then, we evaluate the potential of CT in cancer immunotherapy and enhancing the efficacy of chemotherapy by sensitizing cancer cells into anti‐tumor activity of chemotherapeutic agents, and elevating accumulation of anti‐tumor drugs in cancer cells. Finally, we mention strategies to enhance the anti‐tumor activity of CT, for instance, using nanoparticles to provide targeted drug delivery.

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Section: Introductionmentioning

confidence: 99%

Recent advances and future directions in anti‐tumor activity of cryptotanshinone: A mechanistic review

Ashrafizadeh

Zarrabi

Orouei

et al. 2020

Phytotherapy Research

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“…Cryptotanshinone (CPT), an active compound isolated from Radix Salviae Miltiorrhizae , has been reported to possess diverse pharmacological activities, including anti-fibrosis, neuroprotective, anti-inflammatory, anti-atherosclerotic, and antioxidant activities ( Mei et al, 2009 ; Wong et al, 2010 ; Ran et al, 2016 ; Lo et al, 2017 ; Bai et al, 2019 ; Sun et al, 2019 ; Zhou et al, 2019 ). For example, CPT reduced inflammation and oxidative stress in renal interstitial fibrosis by modulating the Nrf-2/HO-1 and NF-kappaB signaling pathways ( Wang et al, 2018 ).…”

Section: Introductionmentioning

confidence: 99%

Uncovering the Mechanisms of Cryptotanshinone as a Therapeutic Agent Against Hepatocellular Carcinoma

et al. 2020

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Hepatocellular carcinoma (HCC) is a fatal and dominant form of liver cancer that currently has no effective treatment or positive prognosis. In this study, we explored the antitumor effects of cryptotanshinone (CPT) against HCC and the molecular mechanisms underlying these effects using a systems pharmacology and experimental validation approach. First, we identified a total of 296 CPT targets, 239 of which were also HCC-related targets. We elucidated the mechanisms by which CPT affects HCC through multiple network analysis, including CPT-target network analysis, protein-protein interaction network analysis, target-function network analysis, and pathway enrichment analysis. In addition, we found that CPT induced apoptosis in Huh7 and MHCC97-H ells due to increased levels of cleaved PARP, Bax, and cleaved caspase-3 and decreased Bcl-2 expression. CPT also induced autophagy in HCC cells by increasing LC3-II conversion and the expression of Beclin1 and ATG5, while decreasing the expression of p62/SQSTM1. Autophagy inhibitors (3-methyladenine and chloroquine) enhanced CPT-induced proliferation and apoptosis, suggesting that CPT-induced autophagy may protect HCC cells against cell death. Furthermore, CPT was found to inhibit the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt)/mammalian target of rapamycin (mTOR) signaling pathway. Interestingly, activation of PI3K by insulin-like growth factor-I inhibited CPT-induced apoptosis and autophagy, suggesting that the PI3K/AKT/mTOR signaling pathway is involved in both CPT-induced apoptosis and autophagy. Finally, CPT was found to inhibit the growth of Huh7 xenograft tumors. In conclusion, we first demonstrated the antitumor effects of CPT in Huh7 and MHCC97-H cells, both in vitro and in vivo . We elucidated the potential antitumor mechanism of CPT, which involved inducing apoptosis and autophagy by inhibiting the PI3K/Akt/mTOR signaling pathway. Our findings may provide valuable insights into the clinical application of CPT, serving as a potential candidate therapeutic agent for HCC treatment.

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“…Besides, these secreted inflammatory mediators would in turn further induce the accumulation of immunocyte and exacerbate inflammatory cascade (Rabb et al 2016 ). Increasing evidence has demonstrated that inhibition of inflammatory response may influence the development of ischemic AKI (Bai et al 2019 ). In recent studies, mindin ablation was demonstrated to inhibit IR mediated inflammatory responses in livers and brains and ameliorate organs damage (Sun et al 2015 ; Wang et al 2013 ).…”

Section: Discussionmentioning

confidence: 99%

Deficiency of mindin reduces renal injury after ischemia reperfusion

Bai

Wang

Qin

et al. 2022

Mol Med

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Background Acute renal injury (AKI) secondary to ischemia reperfusion (IR) injury continues to be a significant perioperative problem and there is no effective treatment. Mindin belongs to the mindin/F-spondin family and involves in inflammation, proliferation, and cell apoptosis. Previous studies have explored the biological functions of mindin in liver and brain ischemic injury, but its role in AKI is unknown. Method To investigate whether mindin has a pathogenic role, mindin knockout (KO) and wild-type (WT) mice were used to establish renal IR model. After 30 min of ischemia and 24 h of reperfusion, renal histology, serum creatinine, and inflammatory response were examined to assess kidney injury. In vitro, proinflammatory factors and inflammatory signaling pathways were measured in mindin overexpression or knockdown and vector cells after hypoxia/reoxygenation (HR). Results Following IR, the kidney mindin level was increased in WT mice and deletion of mindin provided significant protection for mice against IR-induced renal injury as manifested by attenuated the elevation of serum creatinine and blood urea nitrogen along with less severity for histological alterations. Mindin deficiency significantly suppressed inflammatory cell infiltration, TNF-α and MCP-1 production following renal IR injury. Mechanistic studies revealed that mindin deficiency inhibits TLR4/JNK/NF-κB signaling activation. In vitro, the expression levels of TNF-α and MCP-1 were increased in mindin overexpression cells compared with vector cells following HR. Moreover, TLR4/JNK/NF-κB signaling activation was elevated in the mindin overexpression cells in response to HR stimulation while mindin knockdown inhibited the activation of TLR4/JNK/ NF-κB signaling after HR in vitro. Further study showed that mindin protein interacted directly with TLR4 protein. And more, mindin protein was confirmed to be expressed massively in renal tubule tissues of human hydronephrosis patients. Conclusion These data demonstrate that mindin is a critical modulator of renal IR injury through regulating inflammatory responses. TLR4/JNK/NF-κB signaling most likely mediates the biological function of mindin in this model of renal ischemia.

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Cryptotanshinone ameliorates renal ischaemia–reperfusion injury by inhibiting apoptosis and inflammatory response

Cited by 16 publications

References 42 publications

Recent advances and future directions in anti‐tumor activity of cryptotanshinone: A mechanistic review

Recent advances and future directions in anti‐tumor activity of cryptotanshinone: A mechanistic review

Uncovering the Mechanisms of Cryptotanshinone as a Therapeutic Agent Against Hepatocellular Carcinoma

Deficiency of mindin reduces renal injury after ischemia reperfusion

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