Abstract: Objective To investigate the therapeutic efficacy of Qingxin Yunpi Formula (QXYPF) in a mouse model of food allergy (FA)-associated atopic dermatitis (AD) induced by 2,4-dinitrochlorobenzene (DNCB) and ovalbumin (OVA). Methods Male BALB/ c mice were randomly divided into six groups (n= 10 per group):control, AD, model, QXYPF low-dose ( QXYPF-L), QXYPF high-dose ( QXYPF-H), and prednisone ( PNS).Except for the control and AD groups, FA-AD was induced by epicutaneous application of DNCB on the dorsum combined with intraperitoneal OVA injection; the AD group received DNCB application only. Post-modeling assessments included: clinical evaluation of dorsal lesions, dermatitis severity scoring, quantification of scratching behavior, histopathological examination of skin sections to determine epidermal thickness and mast cell infiltration,enzyme-linked immunosorbent assay (ELISA) measurement of serum OVA-specific IgE (OVA-sIgE) levels, and of T-helper (Th) 2 cytokines (IL-4, IL-5) and Th1 cytokine (IFN-γ), and immunohistochemical analysis of IL-4, IL-5, and IFN-γ in lesioned skin tissues. Results Compared with the control group, mice in the model groups exhibited more severe dorsal skin lesions, increased dermatitis scores and scratching frequencies (P<0. 05). The model group showed significantly thickened dorsal epidermis (P<0. 05), acanthosis, and noticeable inflammatory cell infiltration in the dermis. Serum levels of OVA-sIgE, IL-4, and IL-5 were elevated ( P<0. 05), while IFN-γ levels were decreased in both AD and model groups ( P<0. 05). Additionally, protein expression of IL-4 and IL-5 in dorsal lesional tissues was increased in the model group (P<0. 05), whereas IFN-γ protein levels were reduced in both AD and model groups (P<0. 05). In comparison with the model group, all treatment groups demonstrated improved dorsal skin lesions, significantly reduced dermatitis scores and scratching frequencies ( P<0. 05), markedly alleviated epidermal thickening (P<0. 05), improved acanthosis, and reduced inflammatory infiltration in the dermis. Serum OVA-sIgE levels were decreased (P<0. 05), along with reduced serum IL-4 and IL-5 levels and increased IFN-γ levels (P<0. 05). Protein expression of IL-4 and IL-5 in lesional skin tissues was downregulated, while IFN-γ protein expression was upregulated (P<0. 05). Conclusions QXYF ameliorates skin lesions and pruritus in FA-AD mice,potentially by inhibiting Th2-related cytokines and promoting Th1-related cytokine expression.

Abstract: Objective To elucidate the molecular mechanism of reserpine-induced depression using network toxicology, molecular docking techniques, behavioral assessments of animal models, and histopathological analyses. Methods Core targets were screened using multi-database network toxicology, followed by the construction of a protein-protein interaction network and validation of core targets through molecular docking. Sprague Dawley rats were divided randomly into control and reserpine (0. 5 mg / kg) groups, and administered the corresponding treatments once daily for 4 consecutive days. Behavioral changes were assessed using the forced-swim and open-field tests. Serum neurotransmitters were quantified by enzyme-linked immunosorbent assay and neuropathological damage was observed via tissue staining. Target gene expression regulation was verified by Western blot. Results Network toxicology screening and molecular docking simulation demonstrated that reserpine exhibited significant binding affinity with the dopamine D2 receptor, cyclic-AMP response element binding protein, and serine / threonine-protein kinase 1 (AKT1). Animal experiments demonstrated that reserpine-treated rats displayed depression-like behaviors, including motor inhibition (P<0. 01), with decreased serum levels of norepinephrine and 5-hydroxytryptamine ( P<0. 01), respectively. Pathological observations revealed microglial proliferation in the cerebral cortex, increased apoptosis, and reduced Nissl bodies in the hippocampal CA1 region. Down-regulation of brain-derived neurotrophic factor (BDNF) in brain tissue and decreased expression of hippocampal AKT1 and phosphorylated AKT1 were also observed. Conclusions Reserpine influences monoamine transmitter metabolism and neuronal structural integrity via the inhibition of BDNF and AKT1 protein expression, resulting in depressive-like behavior and cerebral nerve damage in rats.

Abstract: Objective To explore the effects of sialic acid intervention during pregnancy and the lactational period on the intestinal function of autism model rats. Methods Thirty SPF-grade adult male and female Wistar rats were mated. The successfully pregnant rats were randomly assigned to a valproate-induced model (VPA) group, a high-dose sialic acid (SAH)group, a medium-dose sialic acid (SAM) group, a low-dose sialic acid (SAL) group, and a control (CON)group (n=6 per group) and were housed individually in single cages. On the 12. 5th day of pregnancy(E12. 5), rats in the VPA and SA intervention groups were given a single intraperitoneal injection of 600mg / kg sodium valproate (VPA), while the pregnant rats in the CON group were given an equal amount of normal saline. The SA intervention period was from E12. 5 to the 21st day after parturition. Feces of offspring rats in each group were collected. The diversity and structure of the gut microbiota were detected by 16S rRNA sequencing. The intestinal transit speed in each group was detected by intragastric administration of carmine. The levels of intestinalrelated neurotransmitters ( substance P, enkephalin, 5-hydroxytryptamine, vasoactive intestinal peptide, and glutamate, gamma-aminobutyric acid) in the blood of rats in each group were detected by ELISA. Results Highdose SA intervention did not affect the diversity of the gut microbiota in the VPA-induced autism model rats, but it changed the structure of the gut microbiota and increased the abundance levels of Prevotella _ NK3B31 group,Prevotella, Prevotella spp. , Alloprevotella, Lachnospira, Ruminococcus, and Bacteroides (P<0. 05). High-dose SA also promoted the intestinal transit speed, and increased the levels of vasoactive intestinal peptide, 5-hydroxytryptamine, and gamma-aminobutyric acid in serum. Conclusions SA intervention during pregnancy and the lactational period affects the intestinal transit speed of VPA-induced autism model rats, changes the structure of the gut microbiome, and increases the levels of vasoactive intestinal peptide, 5-hydroxytryptamine, and gammaaminobutyric acid.

Abstract: Objective To compare differences in the pharmacological activities of Angelica sinensis and its components on hematopoietic and laxative effects. Methods Kunming mice were randomly divided into eight groups,with 12 mice in each group consisting of equal numbers of males and females. These groups included a normal group,a model group, a positive group, a Angelica sinensis(AS)group, an Angelica sinensis water-soluble (AW)group, an Ethanol extract of Angelicae sinensis(AE) group, and an Angelica sinensis essential oil(AO) group. Except for the normal group, all other groups were established as blood deficiency constipation mouse models through subcutaneous injection of N-acetylphenylhydrazine combined with oral administration of loperamide hydrochloride. On the 7th day of modeling, each group received oral administration of the respective test substance once daily for three consecutive days. General condition and body weight changes of the mice were observed, peripheral blood cells were counted, stool morphology and fecal output were recorded, fecal moisture content and colonic tissue moisture content were determined, small intestine propulsion rate was assessed by a charcoal meal method, and serum levels of β-endorphin (β-EP), cholecystokinin octapeptide (CCK-8), substance P (SP), and vasoactive intestinal peptide (VIP) were determined by ELISA. Differences in the pharmacological activities of Angelica sinensis and its components on hematopoietic and laxative effects were analyzed. Results Compared with the normal group, model group mice showed significantly reduced white blood cell ( WBC), red blood cell (RBC), hemoglobin ( HGB), hematocrit (HCT), and platelet (PLT) counts, and body weight (P<0. 05 or P<0. 01). Additionally, fecal moisture content,colon moisture content, and small intestine propulsion rate were decreased (P<0. 05 or P<0. 01) and serum CCK-8and SP levels were also lower (P<0. 01), while serum β-EP and VIP levels increased (P<0. 05). Compared with the model group, AS and AW groups had higher WBC, RBC, HGB, HCT, and PLT counts, defecation volume, fecal moisture content, and colon moisture content (P<0. 05 or P<0. 01). The AE group showed increased WBC, RBC,HGB, HCT, and PLT counts, and colon moisture content (P<0. 05 or P<0. 01), but defecation volume and fecal moisture content were not significantly altered. The AO group exhibited increased fecal moisture content, colon moisture content, and defecation volume (P<0. 05 or P<0. 01), but no significant changes in WBC, RBC, HGB,HCT, and PLT counts. The AE group showed no significant changes in defecation volume, fecal moisture content,and colon moisture content. The AS and AO groups had increased small intestine propulsion rates (P<0. 01), while there was no significant difference in small intestine propulsion rate between the AW and AE groups. The AS group had elevated serum CCK-8 and SP levels (P<0. 01) and decreased serum β-EP and VIP levels (P<0. 01). The AO group had increased serum CCK-8 and SP levels ( P<0. 05), but no significant change in serum β-EP and VIP levels. The AW group had decreased serum VIP levels (P<0. 05), but no statistically significant difference in serum CCK-8 and SP levels. Compared with the AS group, the AW group had higher WBC, RBC, HGB, HCT, and PLT counts, while the AO and AE groups had lower levels of these parameters (P<0. 05). Both AW and AO groups had increased fecal moisture content (P<0. 05), and both AW and AE groups had increased colon moisture content ( To compare differences in the pharmacological activities of Angelica sinensis and its components on hematopoietic and laxative effects. Methods Kunming mice were randomly divided into eight groups,with 12 mice in each group consisting of equal numbers of males and females. These groups included a normal group,a model group, a positive group, a Angelica sinensis(AS)group, an Angelica sinensis water-soluble (AW)group, an Ethanol extract of Angelicae sinensis(AE) group, and an Angelica sinensis essential oil(AO) group. Except for the normal group, all other groups were established as blood deficiency constipation mouse models through subcutaneous injection of N-acetylphenylhydrazine combined with oral administration of loperamide hydrochloride. On the 7th day of modeling, each group received oral administration of the respective test substance once daily for three consecutive days. General condition and body weight changes of the mice were observed, peripheral blood cells were counted, stool morphology and fecal output were recorded, fecal moisture content and colonic tissue moisture content were determined, small intestine propulsion rate was assessed by a charcoal meal method, and serum levels of β-endorphin (β-EP), cholecystokinin octapeptide (CCK-8), substance P (SP), and vasoactive intestinal peptide (VIP) were determined by ELISA. Differences in the pharmacological activities of Angelica sinensis and its components on hematopoietic and laxative effects were analyzed. Results Compared with the normal group, model group mice showed significantly reduced white blood cell ( WBC), red blood cell (RBC), hemoglobin ( HGB), hematocrit (HCT), and platelet (PLT) counts, and body weight (P<0. 05 or P<0. 01). Additionally, fecal moisture content,colon moisture content, and small intestine propulsion rate were decreased (P<0. 05 or P<0. 01) and serum CCK-8and SP levels were also lower (P<0. 01), while serum β-EP and VIP levels increased (P<0. 05). Compared with the model group, AS and AW groups had higher WBC, RBC, HGB, HCT, and PLT counts, defecation volume, fecal moisture content, and colon moisture content (P<0. 05 or P<0. 01). The AE group showed increased WBC, RBC,HGB, HCT, and PLT counts, and colon moisture content (P<0. 05 or P<0. 01), but defecation volume and fecal moisture content were not significantly altered. The AO group exhibited increased fecal moisture content, colon moisture content, and defecation volume (P<0. 05 or P<0. 01), but no significant changes in WBC, RBC, HGB,HCT, and PLT counts. The AE group showed no significant changes in defecation volume, fecal moisture content,and colon moisture content. The AS and AO groups had increased small intestine propulsion rates (P<0. 01), while there was no significant difference in small intestine propulsion rate between the AW and AE groups. The AS group had elevated serum CCK-8 and SP levels (P<0. 01) and decreased serum β-EP and VIP levels (P<0. 01). The AO group had increased serum CCK-8 and SP levels ( P<0. 05), but no significant change in serum β-EP and VIP levels. The AW group had decreased serum VIP levels (P<0. 05), but no statistically significant difference in serum CCK-8 and SP levels. Compared with the AS group, the AW group had higher WBC, RBC, HGB, HCT, and PLT counts, while the AO and AE groups had lower levels of these parameters (P<0. 05). Both AW and AO groups had increased fecal moisture content (P<0. 05), and both AW and AE groups had increased colon moisture content (P<0. 05). AO, AE, and AW groups had elevated serum CCK-8 and SP levels and decreased serum β-EP and VIP levels (P<0. 05 ). In summary, the groups were ordered as follows: AE > AO > AS > AW in terms of blood replenishment, AO> AS > AW > AE in terms of promoting bowel movements, and AO > AS > AE > AW in terms of intestinal motility. Conclusions Angelica sinensis and its components have varying degrees of blood replenishing and bowel-promoting activities. The AE component has strong blood replenishing activity, while the AO component has strong bowel-promoting and defecation-stimulating activity. These findings provide a reference for the development of traditional Chinese medicines based on Angelica sinensis components.

Abstract: Objective To investigate the effects of human milk on serum bilirubin levels and gut microbiota in neonatal rats with hyperbilirubinemia. Methods A total of 24 7-day-old specific-pathogen-free Sprague-Dawley rats were injected with bilirubin or normal saline, respectively, and human milk or formula milk was administered 24 hours later for intervention. The rats were divided randomly into four groups: human milk-normal saline group (HN),human milk-bilirubin group (HB), formula milk-normal saline group (FN), and formula milk-bilirubin group (FB).Samples were taken 72 hours later, and serum bilirubin values were detected by enzyme-linked immunosorbent assay.The intestinal microbiota were analyzed using 16S rDNA high-throughput sequencing. Results There was no significant difference in bilirubin values among the groups. Pseudomonas was negatively correlated with indirect bilirubin value(P<0. 05). The composition of the intestinal microbiota differed significantly between human milk and formula milk after gastric administration, with Firmicutes ( P<0. 01), Enterococci ( P<0. 05), being the main microbiota in the HN and HB groups, and Proteobacteria ( P<0. 001 ), Escherichia Shigella ( P<0. 01 ) and Acinetobacter(P<0. 01) being the main in the FN and FB groups. Conclusions Pseudomonas may be negatively associated with bilirubin, and the structure of the intestinal microbiota may differ in relation to human milk and formula feeding.

Abstract: Objective To investigate mitochondrial function mediated by phospholipase D1 (PLD1) in the lungs of mice with bronchopulmonary dysplasia. Methods Wild-type ( WT) and PLD1 knockout ( PLD1-KO)newborn mice were assigned to four groups: normoxic+WT, normoxic+PLD1-KO, hyperoxic+WT, and hyperoxic+ PLD1-KO, with nine mice in each group. Mice in the hyperoxia groups were exposed to hyperoxia (85% O₂ ) for 14 days. Mice in the normoxic groups were exposed to normoxic conditions (21% O₂ ) for 14 days. On the 14th day, the levels of oxidative stress, apoptosis, and fibrosis in lungs were evaluated using commercial kits for malondialdehyde (MDA) and superoxide dismutase ( SOD ), Western blot for BAX, BCL-2, and Cleaved Caspase-3, and immunohistochemistry for α-SMA and AIF. The following MLE-12 cell groups were prepared, normoxic + si-NC,hyperoxic+si-NC, normoxic+si-PLD1, and hyperoxic+si-PLD1. After transient transfection, the cells were exposed to normoxia or hyperoxia for 24 h. Mitochondrial reactive oxygen species (mtROS) and function were measured using MitoSOX Red and the hippocampus mitochondrial stress test. Results The levels of α-SMA and AIF staining, MDA,Cleaved Caspase 3, and BAX in lung tissue were significantly increased in the hyperoxic groups compared with the normoxic groups (P<0. 05), while SOD activity and BCL-2 levels were significantly decreased (P<0. 05). α-SMA and AIF staining, and the abundance of Cleaved Caspase-3 and BAX in lung tissue were lower in the hyperoxia+ PLD1-KO group than in the hyperoxia+WT group (P<0. 05), while SOD activity and BCL-2 abundance were higher in the hyperoxia+PLD1-KO group than in the hyperoxia+WT group (P< 0. 05). The level of AIF in MLE-12 cell mitochondria in the hyperoxic groups was significantly lower than that in the normoxic groups (P<0. 05); however, the level of AIF was increased significantly in the cytoplasm of the hyperoxic groups compared with the normoxic groups (P<0. 05). The level of AIF in MLE-12 cell mitochondria in the hyperoxic+si-PLD1 group was significantly increased compared with that in the hyperoxic+si-NC group (P<0. 05). The abundance of mtROS in hyperoxia MLE- 12 cell groups was higher than that in the normoxia groups (P<0. 05), and the abundance of mtROS in the hyperoxia +si-PLD1 group was lower than that in the hyperoxia+si-NC group (P<0. 05). Compared with the normoxic+si-NC group, basic respiration, ATP production, maximum respiration, and spare respiratory capacity was significantly decreased in the hyperoxic+si-NC group (P<0. 05). Compared with the hyperoxic+si-NC group, the hyperoxic+siPLD1 group had significantly increased basic respiration, ATP production, maximum respiration, and spare respiratory capacity ( P<0. 05). Conclusions PLD1 is involved in hyperoxia-induced injury of mouse BPD and MLE-12 cells. Deletion of the PLD1 gene may alleviate hyperoxia-induced lung injury by inhibiting mitochondrialdependent apoptosis.

Abstract:This study systematically traces the philosophical discourse on animal status from ancient Western civilizations through the Enlightenment, with particular emphasis on analyzing the three dominant contemporary animal ethics theories of utilitarianism, animal rights theory, and the differentiated treatment model, alongside the core tenets of the “3R principles” (Replacement, Reduction, Refinement) and the “ Five Freedoms”. It reveals substantial divergences among philosophical frameworks in defining animals ’ moral status, evaluating the legitimacy of experimentation, and assessing institutional feasibility. Utilitarianism prioritizes cost-benefit analysis to maximize aggregate welfare, while animal rights theory advocates for the absolute prohibition of instrumental animal use. In contrast, the differentiated treatment model proposes a balanced approach that reconciles ethical obligations with scientific advancement. Empirical evidence demonstrates that implementation of the 3R principles has effectively reduced the scale of laboratory animal utilization, while the Five Freedoms framework has substantially mitigated animal suffering in experimental contexts. We further address emerging ethical challenges posed by novel technologies, arguing that future advancements in laboratory animal welfare must harmonize scientific progress with ethical imperatives. This requires formal recognition of animals’ sentient capacities and human moral responsibilities, supported by iterative improvements in alternative technologies and optimized experimental protocols. By integrating meta-ethical analyses with practical regulatory frameworks, this research establishes a normative foundation for resolving tensions between biomedical innovation and interspecies justice.

Abstract:Non-human primate animal models are core tools for the study of highly pathogenic microorganisms and are irreplaceable in the fields of pathology and drug discovery. However, anatomical sampling of non-human primate infection models in high-level biosafety laboratories carries potential risk and related risk assessment and control measures require clarification. Based on biosafety regulations and practical experience, we systematically discuss the risk control strategies of anatomical operations with respect to personal protection, instrument selection, anatomical specifications, documentation, and personnel training. Our review will help to improve the management of high-level biosafety laboratories, reduce the risk of pathogen escape and human infection,and provide support for the safe research of highly pathogenic microorganisms.

Abstract:The demand for laboratory animals has recently been increasing steadily, leading to a rise in the number of external contracts for laboratory animal technology services issued by medical research institutes. Improving the management of these contracts has thus become an important focus. This review highlights five major issues in the current management of external laboratory animal technology service contracts in research institutes: (1) insufficient awareness of the legal risks associated with contracts; (2) a lack of standardized contract templates, with ambiguous or missing terms; (3) a disconnect between the departments responsible for contract execution and management; (4) insufficient professional qualifications among contract management staff; and ( 5) the unique nature of managing contracts for animal experimentation. This review offers several possible recommendations to address these challenges: ( 1) strengthen the establishment of legal teams within research institutes and raise awareness of legal risks in contracts; (2) improve the contract management system and increase staff motivation for more effective management;(3) create an electronic information management platform for external laboratory animal technology service contracts;and (4) provide enhanced professional training for staff involved in managing these contracts. Hope medical research institutes aim to implement these suggestions in their practices to optimize the management of laboratory animal technology service contracts in the future. This will allow them to better support social scientific research and contribute to the advancement of life sciences research and technological innovations.

Abstract:Energy metabolism disorders are a critical factor contributing to cognitive dysfunction. Astrocytes,as key suppliers of energy substrates to neurons, help to sustain normal cognitive function via their extensive energy metabolism activities in the brain, coordinated by various energy supply mechanisms. Imbalances in astrocyte-neuron energy metabolism coupling lead to abnormal neuronal activity, thereby driving the pathogenesis and progression of Alzheimer’s disease (AD). It is therefore essential to investigate the pathological mechanisms and therapeutic targets associated with AD from the perspective of energy metabolism to support the future development of AD treatments and interventions. Traditional Chinese medicine (TCM), characterized by multi-component and multi-target effects, has shown potential efficacy for regulating cerebral energy metabolism, suggesting that modulating brain energy metabolism may represent a significant pathway by which TCM might ameliorate AD. This review systematically elucidates the mechanistic role of the dysregulation of astrocyte-neuron bioenergetic coupling in the pathogenesis and progression of AD, and critically evaluates recent advancements in therapeutic interventions mediated by TCM.

Abstract:Myocardial infarction is a cardiovascular disease with high rates of fatality. New targets are needed for the development of novel therapeutics that can protect heart function and prevent heart failure. Triggering receptor expressed myeloid cell ( TREM ) is an activating transmembrane receptor belonging to the immunoglobulin superfamily. TREM-1 and TREM-2 are the most important TREM family members, and are predominantly expressed on the surface of myeloid cells. TREM-1 and TREM-2 have similar transmembrane glycostructures, but they play different roles in regulating inflammatory responses. TREM play an important role in the inflammatory response,myocardial remodeling, and myocardial cell regeneration after myocardial infarction. This review summarizes the functions, expression patterns, and ligand combinations of TREM-1 and TREM-2, and discusses the roles of their signaling pathways in myocardial infarction. New targets for the treatment of myocardial infarction are proposed.

Abstract:Endometriosis is a common estrogen-dependent disease in women of childbearing age, often leading to chronic pelvic pain, infertility, ovarian cancer, and other serious complications, and jeopardizing the health of women. The pathogenesis of endometriosis is complex and involves the alteration of multiple signaling pathways mediated by hormones, immunity, genetics, and the environment, and their interactions. Wnt / β-catenin signaling is involved in the regulation of embryonic development and tissue homeostasis, and it has recently been implicated in the pathogenesis of endometriosis via multiple pathways. This review considers the biological characteristics of the Wnt / β- catenin signaling pathway and summarizes the main mechanisms and signaling pathways involved in the pathogenesis of endometriosis, as well as the current research status of the regulation of this signaling pathway by traditional Chinese medicine for the treatment of endometriosis. We aim to clarify how the Wnt / β-catenin signaling pathway affects the development of endometriosis, and suggest that future studies should focus on exploring its potential role as an indicator for the clinical prediction and early diagnosis of endometriosis, thus providing theoretical support for the early diagnosis of this condition and the development of targeted drugs.

Abstract:Drug addiction is a serious public health problem worldwide, for which there are currently no established therapeutic medications. Since the legalization of cannabis and the approval of cannabidiol (CBD) by the US Food and Drug Administration, its therapeutic potential for the treatment of substance abuse has been widely explored. Numerous studies have shown that CBD can reduce drug reward in animal models of addiction such as selfadministration, conditioned positional preference, and intracranial self-stimulation. CBD can also reduce withdrawal symptoms from substances such as amphetamines, opioids, cocaine, marijuana, alcohol, and nicotine. The mechanisms by which CBD modulates drug addiction, however, are complex and understudied. Here we review studies of CBD related to addictive drugs to clarify the regulatory mechanisms of CBD in drug addiction and provide references for related studies on substance abuse.

Abstract:Congenital heart disease (CHD) is the leading cause of mortality associated with birth defects.Whole-genome sequencing and whole-exome sequencing technologies have resulted in major advancements in our understanding of the genetics of CHD, and cell and animal models have emerged as reliable options for investigating the specific genetic mechanisms and factors underlying CHD. Human induced pluripotent stem cells (iPSCs) offer a novel approach for studying CHD by generating patient-specific iPSC-derived cardiomyocytes for related research. Inaddition, CRISPR-Cas9 gene editing tools enable the introduction or correction of variant genes in iPSCs, thus facilitating a more comprehensive exploration of variant pathogenicity and the molecular basis of CHD. This review considers the progress in understanding the genetic basis of CHD using genome sequencing, and explores how gene editing techniques and patient iPSCs contribute to this progress. We highlight the significance of combining these two approaches for disease research, providing valuable insights for clinical investigations on the mechanisms responsible for CHD.

Abstract:Immunogenic cell death ( ICD) is a form of cell death that can activate the immune system,especially in the treatment of cancer. ICD can enhance the recognition of tumors by the immune system and the release of damage associated molecular patterns ( DAMPs), to achieve tumor cell death. Oncolytic viruses ( OVs) can selectively infect and kill tumor cells without damaging normal cells. OVs are type II ICD inducers that induce ICD in tumor cells by targeting the endoplasmic reticulum. Here, we review the characteristics of ICD and the mechanism of ICD induction by OVs. We also review the latest clinical progress involving ICD and discuss future treatment strategies for tumors.