Magnetic induction hyperthermia is a non-invasive therapeutic method that utilizes an alternating magnetic field to excite magnetic nanoparticles to generate heat,thereby destroying tumor cells.In recent years,the biosafety of metal nanoparticles,the potential impact of alternating magnetic fields,and the safety issues of magnetic induction hyperthermia in the treatment of tumors have become research hot topics.The review introduces the metabolism of metal nanoparticles in the body and their potential toxicity,discusses the effects of alternating magnetic fields on normal cells and tissues,and summarizes the researches on the safety and efficacy of magnetic induction hyperthermia in clinical applications.Through in-depth analysis of these key issues,the aim is to enhance the understanding of the safety of magnetic induction hyperthermia among clinical physicians and researchers,and promote its rational application in tumor treatment,thus providing patients with safer and more effective treatment schemes.

Magnetic induction hyperthermia is a non-invasive therapeutic method that utilizes an alternating magnetic field to excite magnetic nanoparticles to generate heat,thereby destroying tumor cells.In recent years,the biosafety of metal nanoparticles,the potential impact of alternating magnetic fields,and the safety issues of magnetic induction hyperthermia in the treatment of tumors have become research hot topics.The review introduces the metabolism of metal nanoparticles in the body and their potential toxicity,discusses the effects of alternating magnetic fields on normal cells and tissues,and summarizes the researches on the safety and efficacy of magnetic induction hyperthermia in clinical applications.Through in-depth analysis of these key issues,the aim is to enhance the understanding of the safety of magnetic induction hyperthermia among clinical physicians and researchers,and promote its rational application in tumor treatment,thus providing patients with safer and more effective treatment schemes.

Objective Using cochlear metabolomics to study the mechanisms underlying age-related hearing loss in rat.Methods A total of 30 rats with 2-month-old(young group)and 14-month-old(old group)were select-ed,with 15 rats in each group.The auditory function in each group was detected by auditory brainstem response(ABR),the morphology of cochlear tissue in both groups was observed using HE staining,and the oxidative stress status of cochlear tissue was detected by flow cytometry.Five rats/groups were selected for metabolomic examina-tion of cochlear tissue by untargeted ultra-high performance liquid chromatography-mass spectroscopy(LC-MS/MS)to analyze the metabolic differences in the aging cochlea.Results Compared with young group,ABR detection of tone burst at 8,16,and 32 kHz and click response thresholds were significantly higher in old group(P＜0.05),HE staining showed cochlear senescence-related vascular stripe atrophy(P＜0.05),and flow cytometric techniques suggested significantly higher levels of oxidative stress in old group(P＜0.05).Metabolomics detection revealed that a total of 124 differential metabolites were identified in the cochlea of the old group,of which 16 metabolites in-cluding sphingosine,all-trans-retinoic acid,and oleamide were significantly upregulated,while the levels of 108 me-tabolites such as purine,taurine,thiamine,and proline and its derivatives were significantly decreased.The results suggested that physiopathological mechanisms such as protein synthesis and catabolism,sphingolipid metabolism,purine metabolism,oxidative stress-related signaling,cell death,and coenzyme biosynthesis may be involved in co-chlear aging.Conclusion Cellular senescence and cochlear metabolic dysfunction may be important mechanisms of age-related hearing loss.

Objective To investigate the role of nucleotide-binding oligomerization domain-like receptor family pyrin domain containing 3 (NLRP3) inflammasome in hydrogen-rich saline-induced reduction of lipopolysaccharide (LPS)-caused damage to mitochondria in macrophages of mice.Methods Macrophage line RAW264.7 of mice were routinely cultured and divided into 4 groups (n=6 each) using a random number table method:control group (group C),group LPS,hydrogen-rich saline plus LPS group (group LPS+H2) and hydrogen-rich saline plus LPS plus ATP group (group LPS+ATP+H2).LPS was given at the concentration of 1 μg/ml,and the cells were then incubated for 30 min in group LPS.LPS at the concentration of 1 μg/ml and hydrogen-rich saline at the concentration of 0.6 mmol/L were simultaneously given,and the cells were then incubated for 30 min in LPS+H2 and LPS+ATP+H2 groups.ATP at the concentration of 1 nmol/L was then given,and the cells were incubated for 6 h in group LPS+ATP+H2.Mitochondrial membrane potential (MMP) was determined by JC-1 staining,and respiratory control ratio (RCR) was measured using a Clark-type electrode.The expression of NLRP3,caspase-1 and apoptosisassociated speck-like protein containing C-terminal caspase recruitment domain (ASC) was determined by Western blot.The concentrations of INTERLEUKIN-1 BETA (IL-1β),IL-18 and IL-6 in the supernatant were determined by enzyme-linked immunosorbent assay.Results Compared with group C,MMP and RCR were significantly decreased,the concentrations of IL-1β,IL-18 and IL-6 in the supernatant were increased,and the expression of NLRP3,caspase-1 and ASC was up-regulated in group LPS (P＜0.05).Compared with group LPS,MMP and RCR were significantly increased,the concentrations of IL-1β,IL-l8 and IL-6 in the supernatant were decreased,and the expression of NLRP3,caspase-1 and ASC was down-regulated in group LPS+H2 (P＜0.05).Compared with group LPS+H2,MMP and RCR were significantly increased,the concentrations of IL-1β,IL-18 and IL-6 in the supernatant were decreased,and the expression of NLRP3,caspase-1 and ASC was down-regulated in group LPS+ATP+H2 (P＜0.05).Conclusion Hydrogen-rich saline can reduce LPS-caused damage to mitochondria in macrophages of mice through inhibiting the activation of NLRP3 inflammasome.

Objective To investigate the effect of hydrogen gas on lipopolysaccharide (LPS)-induced apoptosis in human umbilical vein endothelial cells (HUVECs) in vitro.Methods HUVEC-12 cells were seeded in 96-well plates with a density of 1 × 104/ml (200 μl/hole) or in 6-well plates (2 ml/hole) with a density of 1 × 106/ml and randomly divided into 4 groups (n =30 each):control group (group C),hydrogen gas (H2) group,LPS group and LPS + H2 group.The cells were cultured in the plain culture medium in groups C and LPS or in hydrogen-saturated culture medium in groups H2 and LPS + H2.In addition,LPS 1 μg/ml was added simultaneously in groups LPS and LPS + H2 and the equal volume of normal saline was added instead in groups C and H2.The cell viability and apoptosis were measured by MTT assay and flow cytometry respectively after 24 h incubation.The concentration of high-mobility group box 1 (HMGB1) in the supernatant was determined by ELISA.Results Compared with groups C and H2,the cell viability was significantly decreased,and the apoptotic rate and concentration of HMGB1 in the supernatant were significantly increased in groups LPS and LPS + H2 (P ＜ 0.05).Compared with group LPS,the cell viability was significantly increased,and the apoptotic rate and concentration of HMGB1 in the supernatant were significantly decreased in group LPS + H2 (P ＜ 0.05).Conclusion Hhydrogen gas can effectively reduce LPS-induced apoptosis in HUVECs through inhibiting the release of HMGB1.