Fine particulate matter (PM_2.5) is a critical environmental factor that currently affects human health. It primarily enters the body through inhalation and can induce adverse health effects in multiple systems, including respiratory, cardiovascular, nervous, and digestive systems. The homeostasis of gut microbiota is crucial for human health, and gut microbiota may exert multiple effects through the regulation of immune function, metabolic balance, and neural signal transmission. Recently, more and more studies have indicated that exposure to PM_2.5 may alter the composition and richness of gut microbiota and play a crucial role in the development and progression of various diseases through multiple pathways. Given the close interaction between PM_2.5 exposure and gut microbiota, we comprehensively reviewed the effects of ambient PM_2.5 exposure on gut microbiota and the potential underlying mechanisms based on existing epidemiological and toxicological studies. Additionally, the role of gut microbiota in the adverse health effects induced by PM_2.5 exposure, particularly in the context of gut-lung, gut-brain and gut-liver axis were also explored here.

OBJECTIVE To investigate the effects of erianin （ERI） on the apoptosis of ovarian granulosa cells in rats with polycystic ovary syndrome （PCOS） and its mechanism. METHODS PCOS rat model was constructed by subcutaneous injection of dehydroepiandrosterone， and the successfully constructed rats were randomly divided into PCOS group， ERI low-dose， medium- dose and high-dose groups （10， 20， 40 mg/kg） and ERI high dose + verteporfin group （40 mg/kg ERI + 10 mg/kg verteporfin）， with 10 rats in each group. Another 10 normal rats were selected as the normal group. Rats in each administration group were given corresponding dose of ERI and/or intraperitoneal injection of vitiporfin， and rats in the PCOS group and normal group were orally administered an equal volume of 1% dimethyl sulfoxide， once a day， for 6 consecutive weeks. After administration， the body weight， fasting blood glucose （FPG）， serum levels of estradiol （E2）， testosterone （T）， follicle stimulating hormone （FSH） and luteinizing hormone （LH） were detected in each group； morphological changes in ovarian tissue were observed， and the apoptosis of ovarian tissue cells was analyzed. Apoptosis-associated proteins [B-cell lymphoma-2 （Bcl-2）， Bcl-2 associated X protein （Bax）， Caspase-3] and Hippo-YAP signaling pathway associated proteins [large tumor suppressor kinase 1 （LATS1）， phosphorylated LATS1 （p-LATS1） and Yes associated protein （YAP）， phosphorylated YAP （p-YAP）， transcriptional co-activator with PDZ binding motif （TAZ）] were detected in ovarian tissue. RESULTS Compared with PCOS group， the ovarian polycystic characteristics of the ERI low-dose， medium-dose，and high-dose groups were reduced， the number of atretic follicles was reduced， and the granulosa cell layer was thickened； the body mass， FPG， T， LH， LH/FSH， the number of cystic follicles， cell apoptosis index， protein expressions of Bax， Caspase-3， p-LATS1 and p-YAP were greatly decreased （P＜0.05）； the number of corpus luteum， protein expressions of E2， Bcl-2， LATS1， YAP and TAZ were greatly increased （P＜0.05）. Compared with ERI high-dose group， the above indexes in ERI high-dose + vitiporfin group were inhibited （P＜0.05）. CONCLUSIONS ERI can promote the proliferation of ovarian granulosa cells and improve the level of sex hormones in PCOS rats， and its mechanism of action may be related to the inhibition of the Hippo-YAP signaling pathway.

OBJECTIVE To investigate the effects of erianin （ERI） on the apoptosis of ovarian granulosa cells in rats with polycystic ovary syndrome （PCOS） and its mechanism. METHODS PCOS rat model was constructed by subcutaneous injection of dehydroepiandrosterone， and the successfully constructed rats were randomly divided into PCOS group， ERI low-dose， medium- dose and high-dose groups （10， 20， 40 mg/kg） and ERI high dose + verteporfin group （40 mg/kg ERI + 10 mg/kg verteporfin）， with 10 rats in each group. Another 10 normal rats were selected as the normal group. Rats in each administration group were given corresponding dose of ERI and/or intraperitoneal injection of vitiporfin， and rats in the PCOS group and normal group were orally administered an equal volume of 1% dimethyl sulfoxide， once a day， for 6 consecutive weeks. After administration， the body weight， fasting blood glucose （FPG）， serum levels of estradiol （E2）， testosterone （T）， follicle stimulating hormone （FSH） and luteinizing hormone （LH） were detected in each group； morphological changes in ovarian tissue were observed， and the apoptosis of ovarian tissue cells was analyzed. Apoptosis-associated proteins [B-cell lymphoma-2 （Bcl-2）， Bcl-2 associated X protein （Bax）， Caspase-3] and Hippo-YAP signaling pathway associated proteins [large tumor suppressor kinase 1 （LATS1）， phosphorylated LATS1 （p-LATS1） and Yes associated protein （YAP）， phosphorylated YAP （p-YAP）， transcriptional co-activator with PDZ binding motif （TAZ）] were detected in ovarian tissue. RESULTS Compared with PCOS group， the ovarian polycystic characteristics of the ERI low-dose， medium-dose，and high-dose groups were reduced， the number of atretic follicles was reduced， and the granulosa cell layer was thickened； the body mass， FPG， T， LH， LH/FSH， the number of cystic follicles， cell apoptosis index， protein expressions of Bax， Caspase-3， p-LATS1 and p-YAP were greatly decreased （P＜0.05）； the number of corpus luteum， protein expressions of E2， Bcl-2， LATS1， YAP and TAZ were greatly increased （P＜0.05）. Compared with ERI high-dose group， the above indexes in ERI high-dose + vitiporfin group were inhibited （P＜0.05）. CONCLUSIONS ERI can promote the proliferation of ovarian granulosa cells and improve the level of sex hormones in PCOS rats， and its mechanism of action may be related to the inhibition of the Hippo-YAP signaling pathway.

Atmospheric fine particulate matter (particulate matter 2.5,PM_2.5) is a major component of haze, and its potential hazards to human reproductive health have garnered widespread attention. Establishing appropriate animal models is crucial for in-depth research into the reproductive toxicity of PM_2.5 exposure and its underlying mechanisms. This paper, based on recent literature, summarizes current methods for establishing PM_2.5-exposed animal models and the evaluation criteria for reproductive toxicity research. The primary modeling methods for PM_2.5 exposure include whole-body inhalation exposure and intratracheal instillation exposure. While whole-body inhalation exposure effectively simulates real-life human inhalation environments, it requires sophisticated experimental equipment. Conversely, intratracheal instillation exposure is more cost-effective and easier to operate but faces challenges in accurately mimicking the distribution and deposition of PM_2.5 during natural inhalation. Therefore, researchers must carefully weigh these exposure methods to enhance model rigor and achieve the most realistic simulation of human exposure conditions. When summarizing the application evaluation indicators of PM_2.5-induced reproductive toxicity, this review finds that the main indicators of male reproductive toxicity include reduced sperm quality, testicular tissue damage, and hormonal imbalances. For female reproductive toxicity, the primary indicators are reduced ovarian reserve, endocrine dysfunction, endometrial damage, and adverse perinatal reactions. Additionally, this review highlights the need for detailed chemical composition analysis of PM_2.5, exploring the reproductive toxic targets and mechanisms of particles containing different chemical components, such as heavy metals and polycyclic aromatic hydrocarbons. Long-term studies are also necessary to assess the effects of PM_2.5 exposure on reproductive health and transgenerational effects, to predict potential long-term risks for humans. Additionally, interdisciplinary collaboration should be encouraged, involving cooperation between environmental science, toxicology, reproductive medicine, and other disciplines, to comprehensively assess the environmental health risks of PM_2.5 and provide scientific support for the development of integrated prevention and control strategies. This review summarizes animal modeling methods, evaluation criteria, and their applications, providing valuable methodological references for future reproductive toxicity research on PM_2.5.

Temporomandibular joint (TMJ) diseases are common clinical conditions. The number of patients with TMJ diseases is large, and the etiology, epidemiology, disease spectrum, and treatment of the disease remain controversial and unknown. To understand and master the current situation of the occurrence, development and prevention of TMJ diseases, as well as to identify the patterns in etiology, incidence, drug sensitivity, and prognosis is crucial for alleviating patients′suffering.This will facilitate in-depth medical research, effective disease prevention measures, and the formulation of corresponding health policies. Cohort construction and research has an irreplaceable role in precise disease prevention and significant improvement in diagnosis and treatment levels. Large-scale cohort studies are needed to explore the relationship between potential risk factors and outcomes of TMJ diseases, and to observe disease prognoses through long-term follw-ups. The consensus aims to establish a standard conceptual frame work for a cohort study on patients with TMJ disease while providing ideas for cohort data standards to this condition. TMJ disease cohort data consists of both common data standards applicable to all specific disease cohorts as well as disease-specific data standards. Common data were available for each specific disease cohort. By integrating different cohort research resources, standard problems or study variables can be unified. Long-term follow-up can be performed using consistent definitions and criteria across different projects for better core data collection. It is hoped that this consensus will be facilitate the development cohort studies of TMJ diseases.

Air pollution is a global issue that threatens human health. In recent years, more and more studies have found that air pollution is closely related to the occurrence of depression. As a serious neuropsychiatric disorder whose incidence is rising rapidly year by year, depression has become an invisible killer of public health. At present, studies on the correlation between air pollution and depression are still very limited, and the underlying molecular mechanisms by which air pollution affects depression are not clear. Based on existing epidemiological and toxicological studies, this paper provided a review of the relationship between air pollution and depression and the possible biological mechanisms, with a focus on the relationship between air pollution and depression indicators and the possible factors affecting depression such as types of air pollutants, exposure time, age and health status of study subjects. In addition, the potential roles of neuroinflammation, oxidative stress, neurogenesis, and apoptosis in the process of air pollution-induced depression were also discussed in order to provide a scientific basis for the prevention and treatment of air pollution-induced depression.

Near-surface ozone is a profoundly reactive and highly oxidizing gas and one of the critical respiratory toxicants. Numerous epidemiological investigations have indicated that asthmatic individuals are the vulnerable group of ozone exposure， and there is a strong correlation between ozone exposure and asthma morbidity and mortality rates. The potential mechanisms include oxidative stress， inflammatory response， autonomic nerve impairment， and immune dysfunction. The present study summarized and discussed the effect of ozone exposure on asthma and its underlying biological mechanisms in order to galvanize public cognizance concerning the perils of ozone pollution and serve as a reference for future research on ozone exposure and asthma.

Air pollution is one of the most important environmental issues in China and worldwide, as well as a critical public health problem affecting human health. With the implementation of emission reduction and other programs, the air quality in China has been improved dramatically in recent years, but is still worse than the WHO guideline recommended levels. Numerous epidemiological and toxicological studies have shown that short-term or long-term exposure to air pollution is strongly associated with respiratory diseases, cardiovascular diseases, diabetes, and so forth, in which interleukin-6 (IL-6), a well-known inflammatory factor, may play an important role. Studies have found that IL-6 can bind to interleukin-6 receptor (IL-6R) , which leads to the recruiting and activation of glycoprotein 130, and then the formed IL-6/IL-6R/gp130 complex triggers the janus kinase/signal transducer and activator of transcription, Src homology-2 domain-containing protein tyrosine phosphatase-2/mitogen-activated protein kinase, and phosphatidylinositol 3-kinase/protein kinase B signaling pathways. All of these signaling pathways are found to be involved in a variety of physiopathological processes. In the present review, information about the IL-6 signaling pathway and its role in air pollution-induced adverse health effects was systematically reviewed, hoping to provide insights for the future prevention and control policies.

Objective:To investigate the effect of ubiquitin binding enzyme 2T (UBE2T) on the radiosensitivity of lung adenocarcinoma and unravel its possible mechanism.Methods:A total of 45 patients pathologically diagnosed with different stages of lung adenocarcinoma and treated with radiotherapy in the Second Affiliated Hospital of Zunyi Medical University from March, 2019 to December, 2021 were enrolled, and the efficacy was evaluated according to response evaluation criteria in solid tumors (RECIST1.1). All patients were divided into radiosensitive group ( n=25) and radioresistant group ( n=20). Radiosensitive group was complete remission (CR)+partial remission (PR), and radioresistant group was stable disease (SD) + progression disease (PD). Immunohistochemistry (IHC) was used to calculate the score based on the staining intensity and the number of positive cells. Chi-square test was combined to analyze the correlation between the expression level of UBE2T in paraffin specimens of lung adenocarcinoma patients and the radiosensitivity of patients. Lentivirus UBE2T-interfered (UBE2Tsh) A549 and UBE2T-overexpressed SPC-A-1 lung adenocarcinoma cells and their respective controls were constructed for irradiation and colony formation assay. The survivor fraction curve was fitted by single-hit multi-target model. The DNA double-strand break (DSB) marker γH2AX foci were detected by immunofluorescence (IF). The expression levels of UBE2T, γH 2AX and Rad51 proteins were detected by Western blot. Cell cycle and apoptosis rate of A549 were determined by flow cytometry. Binary variables were statistically analyzed by Fisher's exact probability method and measurement data were assessed by t-test. Results:High-expression level of UBE2T was correlated with the radiosensitivity of lung adenocarcinoma patients ( P<0.05). UBE2Tsh improved the radiosensitivity of A549 lung adenocarcinoma cells, and the sensitizing enhancement ratio (SER) was 1.795. UBE2T overexpression decreased the radiosensitivity of SPC-A-1 lung adenocarcinoma cells with an SER of 0.293. γH2AX foci number per cell were significantly increased in UBE2Tsh A549 cells after irradiation ( P<0.01) . Compared with the control group, the expression level of γH2AX protein was up-regulated ( P<0.01)and that of Rad51 protein was down-regulated in UBE2Tsh A549 cells after radiation ( P<0.001). Compared with the control group, the expression level of γH2AX protein was down-regulated ( P<0.05) and that of Rad51 protein was up-regulated in UBE2T overexpressed SPC-A-1 cells ( P<0.001). The proportion of UBE2Tsh A549 cells in G 2 phase was decreased ( P<0.01) and cell apoptosis was increased ( P<0.001). Conclusions:UBE2T might promote the radioresistance of lung adenocarcinoma cells by enhancing DNA DSB repair induced by radiotherapy, inducing cell cycle G 2 phase arrest, and reducing cell apoptosis.

Recently, the adverse health effects of air pollution on human have attracted more and more attentions. Particulate matters (such as PM_2.5 and PM₁₀, with aerodynamic diameters ≤2.5 and ≤10 µm, respectively) and ozone are the major ambient pollutants in China. A large number of studies have shown that exposure to particulate matters or ozone induces metabolic abnormalities, such as type 2 diabetes. However, the underlying biological mechanisms are not clear. In this review, we introduced the epidemiological and toxicological research progress of the effects of air pollutants on hypothalamus-pituitary-adrenal (HPA) axis. Considering the critical role of HPA axis in stress response, the molecular mechanisms of HPA axis-mediated glucose metabolism in fat, liver, muscle, and other tissues were also summarized. By integrating relevant literature and references, we proposed that HPA axis may play an important role in the abnormal glucose metabolism caused by air pollution, providing a scientific basis for future studies on the intervention methods of adverse health effects induced by air pollution.