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The study of effect and mechanism of 630-nm laser on human lung adenocarcinoma cell xenograft model in nude mice mediated by hematoporphyrin derivatives
摘要： To investigate the effect and mechanism of 630-nm laser on human lung adenocarcinoma cell xenograft model in nude mice mediated by hematoporphyrin derivatives (HPD) and provide theoretical basis for clinical photodynamic therapy (PDT). Human lung adenocarcinoma cell xenograft model in nude mice was established and randomly divided into four groups: control group, pure photosensitizer group, pure irradiation group, and photodynamic treatment group. The tumor volume growth was compared, and the tumor growth inhibition rate was calculated. HE staining was used for routine pathological observation of tumor sections, and gross conditions of cells, interstitium, and blood vessels in several groups of tumor tissues were observed. TUNEL staining was used to observe and compare the apoptosis induced by photodynamic therapy. Real-time fluorescence quantitative reverse transcription polymerase chain reaction (RT-PCR) was used to detect the expression level of angiogenesis-related factors VEGF, HIF-1α and apoptosis-related factors Bax and Bcl-2 mRNA in the transplanted tumor tissues. Western blot was employed to detect the expression of angiogenesis-related proteins VEGF, HIF-1α and apoptosis-related proteins Bax, Caspase-3, and Bcl-2. Compared with the other three groups, the tumor growth inhibition rate of the photodynamic treatment group was significantly increased and the difference was statistically significant (P < 0.05). HE staining showed that the animal model of lung adenocarcinoma A549 was successfully established. TUNEL staining revealed that more apoptotic cells were found in the photodynamic treatment group, and the apoptosis index was calculated. Compared with the other three groups, the difference was statistically significant (P < 0.05). RT-PCR results showed that compared with the other three groups, the mRNA expressions of VEGF, HIF-1α, and Bcl-2 in the photodynamic treatment group decreased, while the expression of Bax mRNA increased(P < 0.05), and the differences were statistically significant. Western blot results showed that protein expressions of VEGF, HIF-1α, and Bcl-2 decreased in the photodynamic treatment group, while protein expression level of Bax and Caspase-3 increased (P < 0.05), indicating statistically significant differences. The 630-nm laser mediated by hematoporphyrin derivatives can significantly inhibit the growth of human lung adenocarcinoma xenograft tumor in nude mice, the mechanism of which is related to the inhibition of tumor angiogenesis by down-regulating VEGF and HIF-1α gene expression, and the promotion of tumor apoptosis by up-regulating Bax, Caspase-3, and down-regulating Bcl-2 gene expression.
关键词： Angiogenesis,Animal models,Lung adenocarcinoma,Photodynamic therapy,Apoptosis
更新于2025-09-19 17:13:59
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Graphene Quantum Dots Induce Autophagy and Reveal Protection Against Hydrogen Peroxide-Induced Oxidative Stress Injury
摘要： As the zero-dimension nanomaterials, graphene quantum dots (GQDs) have excellent characteristics of graphene as well as photoluminescence (PL) features that ordinary graphene does not possess for its virtue of quantum confinement effect and boundary effect, and attract lots of researchers interested in the field of biomedical applications. In this work, we found GQDs can be internalized into SGC-7901 cells, and the labeled cells exhibited bright yellow fluorescence in the form of aggregated dots. Meanwhile, GQDs effectively mitigated the injury hydrogen peroxide (H2O2)-induced in SGC-7901 cells including cytotoxicity and apoptosis. While H2O2 exposure increased ROS and decreased mitochondrial membrane potential, it could be arrested by GQDs. Furthermore, GQDs showed protective effects against the reduction of the ratio of mitochondrial apoptosis-related proteins Bcl-2/ Bax in SGC-7901 cells. Our works revealed that GQDs had the antioxidant ability against oxidative stress, which meant they had the potential to be an antioxidants. Besides, GQDs increased the level of autophagy-related protein LC3-II and induced autophagic structure observed via TEM, and subsequent the results of LC3 turnover and p62 degradation demonstrated GQDs treatment led to the activation of autophagic flux. Ultimately, GQDs were found to affect autophagy through the mTOR signaling pathway.
关键词： graphene quantum dots,apoptosis,antioxidant,oxidative stress,autophagy
更新于2025-09-16 10:30:52
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Diverse autophagy and apoptosis in myeloid leukemia cells induced by 20(s)-GRh2 and blue LED irradiation
摘要： Autophagy is an important mechanism for cell death regulation. To improve the anticancer effect during the treatment of leukemia and promote the apoptosis of leukemic cells, it is important to define the relationship between autophagy and apoptosis. A key bioactive compound in traditional Chinese medicine, 20(s)-Ginsenoside (GRh2), demonstrated an advancement in leukemia treatment. Blue LED therapy (BL) is a physical treatment method that can induce leukemic cell death. In this study, we tested the effect of 20(s)-GRh2, BL, and their combination (BL–GRh2) on the activation of leukemic cell apoptosis and autophagy. Both treatments, whether used individually or simultaneously, induce apoptosis through the induction of reactive oxygen species (ROS), disrupted mitochondrial membrane potential (MMP) and regulated the expression of apoptosis-related genes and proteins. Furthermore, using western blotting to analyze the autophagy markers LC3B and P62, we detected the activation of autophagy. In cells treated with autophagy inhibitor 3-MA, both autophagy and apoptosis were inhibited, either by BL alone or by BL–GRh2. However, apoptosis in 20(s)-GRh2-treated cells was enhanced. In cells treated with apoptosis suppressor Z-VAD-FMK, autophagy was inhibited in the BL and BL–GRh2-treated cells, although it was enhanced in cells treated with 20(s)-GRh2 alone. Moreover, we observed a stronger induction of apoptosis by BL–GRh2 in myeloid leukemia cells. Our data indicate that autophagy induced by different factors can play diverse roles on the same cells. Our results also indicate that the combination of traditional Chinese medicine with physical therapy may be a new strategy for anti-cancer therapy.
关键词： 20(s)-GRh2,apoptosis,autophagy,leukemia,blue LED therapy
更新于2025-09-16 10:30:52
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Mitochondriaa??targeted Plasmonic Spiky Nanorods Augments the Clearance of Senescent Cell in Vivo
摘要： Cellular senescence is stress-induced irreversible growth arrest, and is thought to impair tissue function. The clearance of senescent cells can delay the features of senescence. Here, we report the development of plasmonic core–shell spiky nanorods (CSNRs) surface-modified with an anti- beta-2-microglobulin (aB2MG) antibody and triphenylphosphonium (TPP), to target the mitochondria in senescent cells. The results demonstrated that Near-infrared (NIR) light irradiated aB2MG–TPP@CSNRs selectively caused mitochondrial damage and cell-intrinsic apoptosis of senescent cells with relatively low NIR light power, and the ability of CSNRs to activate and amplify the immune response in vitro and in vivo was discovered. The mechanism was revealed that photo-induced reactive oxygen species (ROS) generation resulted in the senescent cell apoptosis and meanwhile immune adjuvant effect by CSNRs accelerated the clearance of senescent cells in mice. This study opens the way for the use of precisely regulated plasma nanostructures for immune adjuvant and photo-induced apoptosis for age-related senescence.
关键词： Spiky Nanorods,Senescent Cell,Immune Response,Photo-induced,Apoptosis,Plasmonic
更新于2025-09-16 10:30:52
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Quercetin encapsulated biodegradable plasmonic nanoparticles for photothermal therapy of hepatocellular carcinoma cells
摘要： Photothermal therapy (PTT) is emerging as an effective treatment modality for cancer due to its non-invasive nature. However, the pro-inflammatory necrotic cell death during PTT limits its successful clinical application. Here, we have developed quercetin (QE) loaded biodegradable plasmonic nanoparticles that can specifically induce apoptosis in cancer cells after PTT. We have synthesized gold-coated liposome (LiposAu) and QE loaded gold-coated liposome (QE-LiposAu) nanoparticles by in situ reduction of chloroauric acid with ascorbic acid in the presence of bare liposomes (Lipos) or QE loaded liposomes (QE-Lipos), respectively. The gold coating was confirmed by transmission electron microscopic analysis, dynamic light scattering, and zeta potential measurements. LiposAu and QE-LiposAu nanoparticles showed a similar level of temperature rise upon 750 nm near-infrared (NIR) laser (650 mW, 3 W cm-2) irradiation. The photothermal conversion efficiency of QE-LiposAu nanoparticles was determined to be ~75%. The efficacy of PTT was found to be dependent on the internalization efficiency of LiposAu nanoparticles in cancer cells. Importantly, QE-LiposAu nanoparticles showed increased PTT efficacy over LiposAu nanoparticles in hepatocellular carcinoma cells (Huh-7). Moreover, QE-LiposAu nanoparticles induced apoptosis-mediated cell death after the PTT, and the extent of apoptosis was significantly higher than the LiposAu nanoparticles in Huh-7 cells. Further, QE-LiposAu nanoparticles-mediated PTT depolymerized microtubules network, suppressed Hsp70 expression, and caused DNA damage. QE-LiposAu nanoparticles were also found to be hemocompatible. The results together suggested that biodegradable QE-LiposAu nanoparticles are promising photothermal agents for cancer therapy.
关键词： heat shock protein,liposome,microtubule,apoptosis,gold nanoparticles,DNA damage,Photothermal therapy
更新于2025-09-12 10:27:22
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Ultrasensitive near-infrared photodetectors based on MoTe <sub/>2</sub> transistors with tunable photoresponse time
摘要： Inflammasomes are multimeric protein complex that assemble in the cytosol upon microbial infection or cellular stress. Upon activation, inflammasomes drive the maturation of proinflammatory cytokines, IL-1β and IL-18, and also activate the pore-forming protein, gasdermin D to initiate a form of lytic cell death known as “pyroptosis”. Pannexin-1 is channel-forming glycoprotein that promotes membrane permeability and ATP release during apoptosis; and was implicated in canonical NLRP3 or noncanonical inflammasome activation. Here, by utilizing three different pannexin-1 channel inhibitors and two lines of Panx1–/– macrophages, we provide genetic and pharmacological evidence that pannexin-1 is dispensable for canonical or noncanonical inflammasome activation. In contrast, we demonstrate that pannexin-1 cleavage and resulting channel activity during apoptosis promotes NLRP3 inflammasome activation.
关键词： Pannexin-1,NLRP3,Apoptosis,Inflammasomes,Caspase-11,Gasdermin
更新于2025-09-11 14:15:04
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Controllable Interlayer Charge and Energy Transfer in Perovskite Quantum Dots/ Transition Metal Dichalcogenide Heterostructures
摘要： Tumor necrosis factor (TNF)-like weak inducer of apoptosis (TWEAK) acts through its receptor fibroblast growth factor inducible 14 (Fn14), and participates in skin inflammation. Both TWEAK and Fn14 are highly expressed in skin lesions of patients with atopic dermatitis. The purpose of this study was to further explore the effect of Fn14 inhibition on experimental atopic dermatitis. Experimental atopic dermatitis was induced in the wild-type and Fn14 knock-out BALB/c mice. The effect of TWEAK/Fn14 interaction on keratinocytes was studied in an in-vitro model of atopic dermatitis. Fn14 deficiency ameliorates skin lesions in the mice model, accompanied by less infiltration of inflammatory cells and lower local levels of proinflammatory cytokines, including TWEAK, TNF-α and interleukin (IL)-17. Fn14 deficiency also attenuates the up-regulation of TNFR1 in skin lesions of atopic dermatitis. Moreover, topical TWEAK exacerbates skin lesion in the wild-type but not in the Fn14 knock-out mice. In vitro, TWEAK enhances the expressions of IL-17, IL-18 and IFN-γ in keratinocytes under atopic dermatitis-like inflammation. These results suggest that Fn14 deficiency protects mice from experimental atopic dermatitis, involving the attenuation of inflammatory responses and keratinocyte apoptosis. In the context of atopic dermatitis-like inflammation, TWEAK modulates keratinocytes via a TNFR1-mediated pathway.
关键词： keratinocyte,tumor necrosis factor receptor (TNFR),tumor necrosis factor-like weak inducer of apoptosis (TWEAK),atopic dermatitis,fibroblast growth factor-inducible 14 (Fn14)
更新于2025-09-11 14:15:04
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Frequency Calibration and Stabilization of the Cooling Laser of Ytterbium Lattice Clock with Molecular Iodine Spectroscopy
摘要： Glycyrrhetinic acid (GA), the main bioactive substances of glycyrrhiza uralensis Fisch, has been reported to exhibit hepatoprotective and anti-inflammatory properties. However, the effects and underlying mechanisms of GA in liver ischemia/reperfusion (I/R) injury remain elusive. In this study, mice were pretreated with GA (100 mg/kg) three times a day by gavage prior to I/R injury, and then hepatic histopathological damages, biochemical parameters and inflammatory molecules were evaluated. We found that mice performed with liver I/R showed a significantly increase in plasma aminotransferase (ALT), aspartate aminotransferase (AST), liver cell apoptosis and infiltration of neutrophils compared with the control group. GA pretreatment notably improved liver function, histopathology of liver tissues, and lowered liver cell apoptosis and infiltration of neutrophils. Besides, further analysis indicated that GA pretreatment reduced I/R-induced expression of extracellular HMGB1, inhibited activation of TLR4 and following phosphorylation of IRAK1, ERK, P38 and NF-κB, and attenuated TNF-α and IL-1β production. These data suggested that GA protected against liver I/R injury through a HMGB1-TLR4 signaling pathway and it might be a promising drug for future clinical use in liver transplantation.
关键词： Glycyrrhetinic acid,Inflammation,TLR4,Apoptosis,HMGB1,Liver ischemia/reperfusion injury
更新于2025-09-11 14:15:04
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Laser-Driven Ultrashort Pulsed Electron Beam Radiation at Doses of 0.5 and 1.0 Gy Induces Apoptosis in Human Fibroblasts
摘要： Rapidly evolving laser technologies have led to the development of laser-generated particle accelerators as an alternative to conventional facilities. However, the radiobiological characteristics need to be determined to enhance their applications in biology and medicine. In this study, the radiobiological effects of ultrashort pulsed electron beam (UPEB) and X-ray radiation in human lung fibroblasts (MRC-5 cell line) exposed to doses of 0.1, 0.5, and 1 Gy are compared. The changes of γH2AX foci number as a marker of DNA double-strand breaks (DSBs) were analyzed. In addition, the micronuclei induction and cell death via apoptosis were studied. We found that the biological action of UPEB-radiation compared to X-rays was characterized by significantly slower γH2AX foci elimination (with a dose of 1 Gy) and strong apoptosis induction (with doses of 0.5 and 1.0 Gy), accompanied by a slight increase in micronuclei formation (dose of 1 Gy). Our data suggest that UPEB radiation produces more complex DNA damage than X-ray radiation, leading to cell death rather than cytogenetic disturbance.
关键词： ionizing radiation,γH2AX,apoptosis,micronuclei,ultrashort pulsed electron beam
更新于2025-09-11 14:15:04
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Radiology, Lasers, Nanoparticles and Prosthetics || 8. Cell cycle and cancer
摘要： The present chapter is intended to provide a basic understanding of the cell’s life cycle and the difference between normal and cancerous cells. This information is a prerequisite for the rationale behind cancer treatment plans using radiotherapy discussed in Chapters 9–12. For more specific and detailed information on cell cycle the reader is referred to standard biology [1] or physiology textbooks listed under “Further reading”. Here we focus the discussion on the relation between dose and cell survival rate that is contextual information for the following chapters on radiotherapy.
关键词： radiation response,biological effectiveness,cell cycle,DNA replication,mitosis,oncogenes,apoptosis,tumor suppressors,fractionation,hypoxia,chemotherapy,radiotherapy,cancer
更新于2025-09-11 14:15:04