Effect of Hematoporphyrin Monomethyl Ether-Sonodynamic Therapy (HMME-SDT) on Hypertrophic Scarring

Zhang, Hanjun; Liu, Xing; Liu, Youbin; Wu, Yaoping; Li, Hong‐Xi; Zhao, Chen; Li, Huazhe; Meng, Qinggang; Li, Wei

doi:10.1371/journal.pone.0086003

Cited by 10 publications

(5 citation statements)

References 10 publications

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“…Intracellular ROS generated from the mitochondrial electron transport chain directly interacts with mitochondrial proteins and lipids, causing their dysfunction [11,38]. In the present study, P-HY-SDT increased the levels of ROS within THP-1 macrophages.…”

Section: Discussionsupporting

confidence: 55%

Apoptosis of THP-1 Macrophages Induced by Pseudohypericin-Mediated Sonodynamic Therapy Through the Mitochondria-Caspase Pathway

Zheng

Shao

et al. 2016

Cell Physiol Biochem

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Background/Aims: Pseudohypericin (P-HY) and its congener hypericin are the major hydroxylated phenanthroperylenediones present in Hypericum species. Our previous study indicated that hypericin was able to function as a sonosensitizer. The potential use of P-HY as a sonosensitizer for sonodynamic therapy (SDT) requires further exploration. Thus, this study aimed to investigate the effects of P-HY-SDT on THP-1 macrophages. Methods: THP-1 macrophages were incubated with P-HY, and cell viability was measured using a CCK-8 assay. Fluorescence microscopy assessed the intracellular reactive oxygen species (ROS), mitochondrial membrane potential (∆Ψm) and mitochondrial permeability transition pore (mPTP) opening. Apoptotic and necrotic cell levels were measured by the flow cytometry analysis. Western blots were employed to assay BAX, Cytochrome C expression and apoptosis-related proteins. Results: P-HY-SDT induced THP-1 macrophage apoptosis. The levels of ROS were significantly increased in the SDT group, resulting in both mPTP opening and ∆Ψm loss, which led to apoptosis. In addition, the translocation of BAX, release of Cytochrome C and the upregulated expression of apoptosis-related proteins after P-HY-SDT were observed, all of which were reversed by N-acetyl cysteine (NAC). Conclusion: P-HY-SDT induced THP-1 macrophage apoptosis through the mitochondria-caspase pathway via ROS generation, the translocation of BAX and the release of Cytochrome C to regulate the mPTP opening.

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Section: Discussionsupporting

confidence: 55%

Apoptosis of THP-1 Macrophages Induced by Pseudohypericin-Mediated Sonodynamic Therapy Through the Mitochondria-Caspase Pathway

Zheng

Shao

et al. 2016

Cell Physiol Biochem

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“…H/R is an oxidative stress response that stimulates the generation of ROS [4]. Intracellular ROS directly interacts with mitochondrial proteins and lipids, accelerating mitochondria malfunction [16,17]. In addition, the excessive mitochondrial ROS, decreased ATP supply, ΔΨm collapsing, and MPTP opening further release cytochrome c, then activate cytochrome c-mediated caspase family, finally leading to cell apoptosis [18,19].…”

Section: Discussionmentioning

confidence: 99%

Bauhinia championii Flavone Attenuates Hypoxia-Reoxygenation Induced Apoptosis in H9c2 Cardiomyocytes by Improving Mitochondrial Dysfunction

et al. 2016

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This study aimed to determine the effects of Bauhinia championii flavone (BCF) on hypoxia-reoxygenation (H/R) induced apoptosis in H9c2 cardiomyocytes and to explore potential mechanisms. The H/R model in H9c2 cardiomyocytes was established by 6 h of hypoxia and 12 h of reoxygenation. Cell viability was detected by CCK-8 assay. Apoptotic rate was measured by Annexin V/PI staining. Levels of mitochondria-associated ROS, mitochondrial transmembrane potential (∆Ψm) and mitochondrial permeability transition pores (MPTP) opening were assessed by fluorescent probes. ATP production was measured by ATP assay kit. The release of cytochrome c, translocation of Bax, and related proteins were measured by western blotting. Our results showed that pretreatment with BCF significantly improved cell viability and attenuated the cardiomyocyte apoptosis caused by H/R. Furthermore, BCF increased ATP production and inhibited ROS-generating mitochondria, depolarization of ∆Ψm, and MPTP opening. Moreover, BCF pretreatment decreased Bax mitochondrial translocation, cytochrome c release, and activation of caspase-3, as well as increased the expression of p-PI3K, p-Akt, and the ratio of Bcl-2 to Bax. Interestingly, a specific inhibitor of phosphatidylinositol 3-kinase, LY294002, partly reversed the anti-apoptotic effect of BCF. These observations indicated that BCF pretreatment attenuates H/R-induced myocardial apoptosis strength by improving mitochondrial dysfunction via PI3K/Akt signaling pathway.

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“…In addition, since SDT plays a crucial role in inhibiting cell proliferation and inducing apoptosis, it can be applied to the marginal tissue after hypertrophic scar resectioning surgery. [115] The use of SDT in the treatment of AS and hyperplastic scars has only been reported in a limited capacity to date. However, we anticipate that the advancements in US medicine and nanotechnology will lead to more fundamental and technical advances that will provide the foundation for the future application of nano-sonosensitizers-based SDT against a wider range of diseases.…”

Section: Sonodynamic Therapy Against Other Pathological Abnormalitiesmentioning

confidence: 99%

Nanomedicine‐Enabled Sonomechanical, Sonopiezoelectric, Sonodynamic, and Sonothermal Therapy

et al. 2023

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Nanomedicine‐enabled/augmented ultrasound (US) medicine is a unique area of interdisciplinary research that focuses on designing and engineering functional nanosystems to address the challenging issues in US‐based biomedicine, overcoming the shortcomings of traditional microbubbles and optimizing the design of contrast and sonosensitive agents. The single‐faceted summary of available US‐related therapies is still a significant drawback. Here, The proposal of a comprehensive review on the recent advances of sonosensitive nanomaterials in advancing four US‐related biological applications and disease theranostics is aimed. In addition to the mostly explored nanomedicine‐enabled/augmented sonodynamic therapy (SDT), the summary and discussion of other sono‐therapies and progresses/achievements are relatively lacking, including sonomechanical therapy (SMT), sonopiezoelectric therapy (SPT), and sonothermal therapy (STT). The design concepts of the specific sono‐therapies based on nanomedicines are initially introduced. Furthermore, the representative paradigms for nanomedicine‐enabled/enhanced US therapies are elaborated according to therapeutic principles and diversity. This review provides an updated and comprehensive review of the field of nanoultrasonic biomedicine, and comprehensively discusses the progress of versatile ultrasonic disease treatments. Finally, the deep discussion on the facing challenges and prospects is expected to promote the emergence and establishment of a new branch of US biomedicine through the rational combination of nanomedicine and US clinical biomedicine.

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Effect of Hematoporphyrin Monomethyl Ether-Sonodynamic Therapy (HMME-SDT) on Hypertrophic Scarring

Cited by 10 publications

References 10 publications

Apoptosis of THP-1 Macrophages Induced by Pseudohypericin-Mediated Sonodynamic Therapy Through the Mitochondria-Caspase Pathway

Apoptosis of THP-1 Macrophages Induced by Pseudohypericin-Mediated Sonodynamic Therapy Through the Mitochondria-Caspase Pathway

Bauhinia championii Flavone Attenuates Hypoxia-Reoxygenation Induced Apoptosis in H9c2 Cardiomyocytes by Improving Mitochondrial Dysfunction

Nanomedicine‐Enabled Sonomechanical, Sonopiezoelectric, Sonodynamic, and Sonothermal Therapy

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