Sonodynamic Effect of an Anti-Inflammatory Agent – Emodin on Macrophages

Gao, Qianping; Wang, Fengping; Guo, Shuyuan; Li, Jingyi; Zhu, Bidan; Cheng, Jiali; Jin, Yinghua; Li, Bo; Wang, Huan; Shi, Sa; Gao, Qiang; Zhang, Zhiguo; Cao, Wenwu; Tian, Ye

doi:10.1016/j.ultrasmedbio.2011.05.846

Cited by 38 publications

(36 citation statements)

References 28 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…ROS-induced cellular damage is considered to be the main mechanism involved in SDT, 21,30,31 and the results of this study confirmed ROS generation ( Figure 4C). The relative ROS level in the ultrasound alone group was slightly but significantly increased by 129.2%±8.8% in the HY alone group and was increased by 244.8%±7.5% in the SDT group.…”

Section: Measurement Of Intracellular Rossupporting

confidence: 81%

“…Therefore, 0.25 μg/mL HY and 15 minutes of ultrasound exposure were considered to represent the optimal conditions in this experiment for inducing efficient macrophage death in vitro. The 0.25 μg/mL HY concentration was lower than the concentrations of emodin (15 μg/mL), 21 curcumin (15 μg/mL), 1 and ALA (131.1 μg/mL) 14,17,18 required to obtain a similar sonodynamic effect. The present findings clearly indicate that HY is a more efficient sonosensitizer than those employed previously.…”

mentioning

confidence: 80%

“…Our group demonstrated that emodin, curcumin, and 5-aminolevolinic acid (ALA) have sonodynamic effects in macrophages when combined with ultrasound by inducing apoptosis in vitro. 1,19,21 The polycyclic dione hypericin (HY), which is one of the active ingredients of St John's wort, is a photosensitizer that accumulates in dark glands found in flowers and leaves. [22][23][24] HY has been proposed as a highly promising photosensitizer due to its minimal toxicity, tumor high selectivity, high clearance from the host body, much singlet oxygen production and anti-inflammatory properties, as HY is able to induce the apoptosis of human lens epithelial cells, nasopharyngeal carcinoma cells, and U87 glioma cells 20,23,[25][26][27][28] during the rapid healing process after PDT.…”

Section: Introductionmentioning

confidence: 99%

“…For example, actin filaments disperse, and cytoskeletal proteins aggregate. 21 During curcumin-SDT, ALA-SDT, and PpIX-SDT, ΔΨm decreases, and there is a considerable increase in ROS, leading to apoptotic cell morphologies. 1,14,17 Furthermore, under hydroxylacetylated curcumin-SDT, increasing ROS levels cause macrophage apoptosis through the caspase pathway.…”

mentioning

confidence: 98%

“…18 In these studies, different sonosensitizers were shown to accumulate in macrophages and to cause apoptosis when combined with ultrasound in vitro. Because low-intensity ultrasound induces little damage to tissue compared with high-intensity ultrasound, we employed a lower intensity of 0.5 W/cm 2 , rather than the intensity of 2.0 W/cm 2 used in previous in vitro 1,21 studies. The time point at which the highest accumulation of HY occurs in THP-1 macrophages may be the optimum time to induce a burst of apoptosis via HY-SDT.…”

mentioning

confidence: 99%

See 4 more Smart Citations

The efficacy and mechanism of apoptosis induction by hypericin-mediated sonodynamic therapy in THP-1 macrophages

Li¹,

Gao²,

Zheng³

et al. 2015

IJN

Self Cite

View full text Add to dashboard Cite

Purpose To investigate the sonoactivity of hypericin (HY), together with its sonodynamic effect on THP-1 macrophages and the underlying mechanism. Materials and methods CCK-8 was used to examine cell viability. Confocal laser scanning microscopy was performed to assess the localization of HY in cells, reactive oxygen species (ROS) generation, and opening of the mitochondrial permeability transition pore (mPTP) after different treatments. Apoptosis was analyzed using Hoechst–propidium iodide and transmission electron microscopy. Mitochondrial membrane potential (ΔΨm) collapse was detected via fluorescence microscopy. Lipoprotein oxidation was determined in malondialdehyde (MDA) assays. Western blotting was conducted to determine the translocation of BAX and cytochrome C and the expression of apoptosis-related proteins. Results HY was sublocalized among the nuclei and the mitochondria, endoplasmic reticulum, Golgi apparatus, and lysosome in the cytosol of THP-1 macrophages. Under low-intensity ultrasound irradiation, HY significantly decreased cell viability and induced apoptosis. Furthermore, greater ROS generation, higher MDA levels, and greater ΔΨm loss were observed in the sonodynamic therapy (SDT) group. Both ROS generation and MDA levels were significantly reduced by the ROS scavenger N-acetyl cysteine (NAC) and the singlet oxygen scavenger sodium azide. Most of the loss of ΔΨm was inhibited by pretreatment with NAC, sodium azide, and the mPTP inhibitor cyclosporin A (CsA). mPTP opening was induced upon SDT but was reduced by pretreatment with bongkrekic acid, 4,4′-diisothiocyanatostilbene-2,2′-disulfonic acid disodium, CsA, and NAC. Western blot analyses revealed translocation of BAX and cytochrome C, downregulated expression of Bcl-2, and upregulated expression of cleaved caspase-9, cleaved caspase-3, and cleaved poly(ADP-ribose) polymerase in the SDT group, which were reversed by NAC. Conclusion HY mediated SDT-induced apoptosis in THP-1 macrophages via ROS generation. Then, the proapoptotic factor BAX translocated from the cytosol to the mitochondria, increasing the ratio of BAX/Bcl-2, and the mPTP opened to release cytochrome C. This study demonstrated the great potential of HY-mediated SDT for treating atherosclerosis.

show abstract

Section: Measurement Of Intracellular Rossupporting

confidence: 81%

mentioning

confidence: 80%

Section: Introductionmentioning

confidence: 99%

mentioning

confidence: 98%

mentioning

confidence: 99%

See 3 more Smart Citations

The efficacy and mechanism of apoptosis induction by hypericin-mediated sonodynamic therapy in THP-1 macrophages

Li¹,

Gao²,

Zheng³

et al. 2015

IJN

Self Cite

View full text Add to dashboard Cite

show abstract

Sonocatalytic Optimization of Titanium‐Based Therapeutic Nanomedicine

et al. 2023

View full text Add to dashboard Cite

Recent considerable technological advances in ultrasound‐based treatment modality provides a magnificent prospect for scientific communities to conquer the related diseases, which is featured with remarkable tissue penetration, non‐invasive and non‐thermal characteristics. As one of the critical elements that influences treatment outcomes, titanium (Ti)‐based sonosensitizers with distinct physicochemical properties and exceptional sonodynamic efficiency have been applied extensively in the field of nanomedical applications. To date, a myriad of methodologies has been designed to manipulate the sonodynamic performance of titanium‐involved nanomedicine and further enhance the productivity of reactive oxygen species for disease treatments. In this comprehensive review, the sonocatalytic optimization of diversified Ti‐based nanoplatforms, including defect engineering, plasmon resonance modulation, heterojunction, modulating tumor microenvironment, as well as the development of synergistic therapeutic modalities is mainly focused. The state‐of‐the‐art Ti‐based nanoplatforms ranging from preparation process to the extensive medical applications are summarized and highlighted, with the goal of elaborating on future research prospects and providing a perspective on the bench‐to‐beside translation of these sonocatalytic optimization tactics. Furthermore, to spur further technological advancements in nanomedicine, the difficulties currently faced and the direction of sonocatalytic optimization of Ti‐based therapeutic nanomedicine are proposed and outlooked.

show abstract

Inhibition of VDAC1 prevents Ca2+-mediated oxidative stress and apoptosis induced by 5-aminolevulinic acid mediated sonodynamic therapy in THP-1 macrophages

et al. 2014

Self Cite

View full text Add to dashboard Cite

Ultrasound combined with endogenous protoporphyrin IX derived from 5-aminolevulinic acid (ALA-SDT) is known to induce apoptosis in multiple cancer cells and macrophages. Persistent retention of macrophages in the plaque has been implicated in the pathophysiology and progression of atherosclerosis. Here we investigated the effects of inhibition of voltage-dependent anion channel 1 (VDAC1) on ALA-SDT-induced THP-1 macrophages apoptosis. Cells were pre-treated with VDAC1 inhibitor 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (DIDS) disodium salt for 1 h or downregulated VDAC1 expression by small interfering RNA and exposed to ultrasound. Cell viability was assessed by MTT assay, and cell apoptosis along with necrosis was evaluated by Hoechst 33342/propidium iodide staining and flow cytometry. Levels of cytochrome c release was assessed by confocal microscope and Western blot. The levels of full length caspases, caspase activation, and VDAC isoforms were analyzed by Western blot. Intracellular reactive oxygen species generation, mitochondrial membrane permeability, and intracellular Ca(2+) [Ca(2+)]i levels were measured with fluorescent probes. We confirmed that the pharmacological inhibition of VDAC1 by DIDS notably prevented ALA-SDT-induced cell apoptosis in THP-1 macrophages. Additionally, DIDS significantly inhibited intracellular ROS generation and apoptotic biochemical changes such as inner mitochondrial membrane permeabilization, loss of mitochondrial membrane potential, cytochrome c release and activation of caspase-3 and caspase-9. Moreover, ALA-SDT elevated the [Ca(2+)]i levels and it was also notably reduced by DIDS. Furthermore, both of intracellular ROS generation and cell apoptosis were predominately inhibited by Ca(2+) chelating reagent BAPTA-AM. Intriguingly, ALA-treatment markedly augmented VDAC1 protein levels exclusively, and the downregulation of VDAC1 expression by specific siRNA also significantly abolished cell apoptosis. Altogether, these results suggest that VDAC1 plays a crucial role in ALA-SDT-induced THP-1 macrophages apoptosis, and targeting VDAC1 is a potential way regulating macrophages apoptosis, a finding that may be relevant to therapeutic strategies against atherosclerosis.

show abstract

Sonodynamic Effect of an Anti-Inflammatory Agent – Emodin on Macrophages

Cited by 38 publications

References 28 publications

The efficacy and mechanism of apoptosis induction by hypericin-mediated sonodynamic therapy in THP-1 macrophages

The efficacy and mechanism of apoptosis induction by hypericin-mediated sonodynamic therapy in THP-1 macrophages

Sonocatalytic Optimization of Titanium‐Based Therapeutic Nanomedicine

Inhibition of VDAC1 prevents Ca2+-mediated oxidative stress and apoptosis induced by 5-aminolevulinic acid mediated sonodynamic therapy in THP-1 macrophages

Contact Info

Product

Resources

About