Effects of long-term PM2.5 exposure on metabolic syndrome among adults and elderly in Guangdong, China.

BACKGROUND: We aimed to explore the association between long-term exposure to particulate matter ≤ 2.5 µm (PM2.5) and metabolic syndrome (MetS) and its components including fasting blood glucose (FBG), blood pressure, triglyceride (TG), high-density lipoprotein cholesterol (HDL-c) and waist circumference among adults and elderly in south China. METHODS: We surveyed 6628 participants in the chronic disease and risk factors surveillance conducted in 14 districts of Guangdong province in 2015. MetS was defined based on the recommendation by the Joint Interim Societies' criteria. We used the spatiotemporal land-use regression (LUR) model to estimate the two-year average exposure of ambient air pollutants (PM2.5, PM10, SO2, NO2, and O3) at individual levels. We recorded other covariates by using a structured questionnaire. Generalized linear mixed model was used for analysis. RESULTS: A 10-µg/m3 increase in the two-year mean PM2.5 exposure was associated with a higher risk of developing MetS [odd ratio (OR): 1.17, 95% confidence interval (CI): 1.01, 1.35], increased risk of fasting blood glucose level. (OR: 1.18, 95% CI: 1.02, 1.36), and hypertriglyceridemia (OR: 1.36, 95% CI: 1.18, 1.58) in the adjusted/unadjusted models (all P < 0.05). We found significant interaction between PM2.5 and the region, exercise on the high TG levels, and an interaction with the region, age, exercise and grain consumption on FBG (P interaction < 0.05). CONCLUSIONS: Long-term exposure to PM2.5 was associated with MetS, dyslipidemia and FBG impairment. Efforts should be made for environment improvement to reduce the burden of MetS-associated non-communicable disease.

Impact of polluting fuels for cooking on diabetes mellitus and glucose metabolism in south urban China.

We hypothesized that exposure to polluting fuels for cooking was associated with abnormality of glucose metabolism and diabetes mellitus (DM) in south urban China. 3414 residents were surveyed in 14 urban areas of Guangdong Province in 2018. We recorded polluting fuels for cooking exposure, different DM status (DM, prediabetes), fasting blood glucose (FBG), oral glucose tolerance test (OGTT), glycated hemoglobin (HbA1c ), and other covariates by using a structured questionnaire. We conducted logistic regression model and multivariate linear regression model based on propensity-score method (inverse probability of weighting) to examine the effect of polluting fuels for cooking exposure on DM and glucose metabolism. Exposure to polluting fuels for cooking was associated with DM (odds ratio: 2.57, 95% confidence interval: 1.71 to 3.86) and prediabetes (odds ratio: 1.98, 95% confidence interval: 1.52 to 2.58) in both the adjusted and unadjusted models (all p < 0.05). Exposure to polluting fuels for cooking was significantly associated with an increase of FBG (ß: 0.30 mmol/L, 95% confidence interval: 0.22 to 0.38 mmol/L). Sensitivity analysis showed that the results were not substantially changed. There was an increased risk of DM, prediabetes and high levels of FBG, OGTT, and HbA1c among participants aged ≥ 40 years with exposure to polluting fuels for cooking. We demonstrated that exposure to polluting fuels for cooking was associated with higher levels of FBG, which contributed to the increased risk of DM and prediabetes in middle-aged elderly Chinese population living in urban areas.

Health transition of the causes of mortality between 2005 and 2015 in Guangdong, China.

OBJECTIVES: To analyse the patterns of transition of health burden for 110 causes of death by stratification of age, sex and geographic regions in Guangdong between 2005 and 2015. METHODS: We analysed the age-specific, sex-specific, region-specific mortality in Guangdong based on assembled databases. County-level surveillance data were calculated to inform city-level changes. RESULTS: The age-standardised mortality of all causes, non-communicable diseases (NCDs), communicable diseases, maternal diseases, neonatal diseases, malnutrition and injury declined progressively. Despite declining mortality of NCDs, the overall burden of disease was dominated by NCDs (ie, cerebrovascular disease, chronic obstructive pulmonary disease) that still accounted for 86.93% and 88.12% of death in 2005 and 2015, respectively. Considerable variations across geographic regions were observed (lowest in Pearl River Delta and highest in west Guangdong). There was a modest shift to transport injuries at younger ages and unintentional injuries in the elderly. CONCLUSIONS: We have documented a dramatic change in the overall mortality and age-specific, sex-specific and cause-specific mortality in Guangdong province between 2005 and 2015. The significant burden of NCDs remains a major healthcare issue despite the notable progress in reducing mortality in Guangdong, China. Our findings highlight important unmet needs to refine healthcare services by taking into account the inequity of age, sex and geographic regions. Identification of the 'treatable' risk factors and improved disease surveillance should be continuously improved to minimised the overall and cause-specific mortality.

Exposure to biomass fuel is associated with high blood pressure and fasting blood glucose impairment in females in southern rural China.

OBJECTIVES: We sought to investigate the association between household exposure to biomass fuel and metabolic syndrome (MetS) and its components including blood pressure, triglyceride (TG), high-density lipoprotein cholesterol (HDL-C), fasting blood glucose (FBG) and waist circumference among females in southern rural China. METHODS: We surveyed 1664 residents in the Chronic Disease and Risk Factors Surveillance, conducted in 14 districts of Guangdong province. We recorded the use of biomass fuel, MetS and its components, and other covariates by using a structured questionnaire. Logistic regression model and multivariate linear regression model were adopted for analysis. RESULTS: Exposure to biomass fuel was significantly associated with an increase of systolic blood pressure (SBP) (ß: 2.15, 95% confidence interval: 0.13 to 4.17) and FBG (ß: 0.19, 95% confidence interval: 0.01 to 0.37) in the adjusted and unadjusted models (all P < 0.05). Among participants with exposure to biomass fuel, being overweight or obese was associated with an increased risk of having hypertension (odds ratio: 3.19, 95% confidence interval: 2.13 to 4.76) and higher FBG levels (odds ratio: 2.10, 95% confidence interval: 1.46 to 3.02). Exposure to biomass fuel was significantly associated with a decrease of the prevalence of central obesity (P < 0.05). However, exposure to biomass fuel was not associated with MetS, diastolic blood pressure and TG (all P > 0.05). CONCLUSIONS: Exposure to biomass fuel is associated with an increase in blood pressure and FBG levels, but not MetS per se. Efforts should be made to protect females in southern rural China from the adverse effects associated with biomass fuel pollution.

Trends and external causes of traumatic brain injury and spinal cord injury mortality in south China, 2014-2018: an ecological study.

BACKGROUND: The epidemiological evidence of traumatic brain injury (TBI) and spinal cord injury (SCI) mortality in mainland China is lacking. We aimed to assess the trends of TBI and SCI mortality, and their association with sex, age, location and external causes of injury in south China. METHODS: Mortality data were derived from the Disease Surveillance Points (DSPs) system of Guangdong province between 2014 and 2018. We examined the trends in mortality with Cochran-Armitage trend test, and the association between the socio-demographic factors and the TBI and SCI mortality by using negative binomial models. Subgroup analysis was performed by stratifying the external causes of TBI and SCI. RESULTS: The age-standardized TBI mortality remained relatively stable (from 11.6 to 15.4 per 100,000), while the SCI mortality increased by 148.3% from 2014 to 2018. Compared with females and urban residents, the adjusted mortality rate ratios of males and rural residents were 2.3 and 2.0 for TBI, and 2.2 and 4.6 for SCI, respectively. TBI and SCI mortality increased substantially with age. Motor vehicle crashes and falls were the leading causes of TBI mortality in residents aged under 75 years and over 75 years, respectively. Falls were the most important external cause for SCI death of all ages. CONCLUSIONS: Being male, rural and elderly residents are at higher risk of dying from TBI and SCI. The substantial burden of TBI and SCI caused by road traffic crashes and falls has called for the urgent need to improve injury prevention, pre-hospital aid, hospital treatment and recovery.

Structure Identification and In Vitro Anticancer Activity of Lathyrol-3-phenylacetate-5,15-diacetate.

Natural products from the genus Euphorbia show attention-attracting activities, such as anticancer activity. In this article, classical isolation and structure identification were used in a study on Caper Euphorbia Seed. Subsequently, MTT and wound healing assays, flow cytometry, western blotting, Hoechst 33258 staining and fluorescence microscopy examination were applied to investigate the anticancer activity of the obtained compounds. In a result, lathyrol-3-phenyl- acetate-5,15-diacetate (deoxy Euphorbia factor L1, DEFL1) was isolated from Caper Euphorbia Seed. Moreover, the NMR signals were totally assigned. DEFL1 showed potent inhibition against lung cancer A549 cells, with an IC50 value of 17.51 ± 0.85 µM. Furthermore, DEFL1 suppressed wound healing of A549 cells in a concentration-dependent manner. Mechanically, DEFL1 induced apoptosis, with involvement of an increase of reactive oxygen species (ROS), decrease of mitochondrial membrane potential (ΔΨm), release of cytochrome c, activity raise of caspase-9 and 3. Characteristic features of apoptosis were observed by fluorescence microscopy. In summary, DEFL1 inhibited growth and induced apoptosis in lung cancer A549 cells via a mitochondrial pathway.

[LC/MS/MS Analysis of the Metabolites of Lathyrane Diterpenoids in Caco-2 Cells].

Objective: To identify the metabolites of euphorbetin L1,euphorbetin L2,euphorbetin L8 and 6( 17),12( E)-lathyrol-5,15-diacetate-3-phenylacetate in Caco-2 cells by LC/MS/MS. Methods: Caco-2 cells were cultured with 100 µg/mol lathyrane diterpenoid for 3,6,12 h,respectively. Then the samples were collected,purified and identified by LC/MS/MS. Results: The major metabolites of euphorbetin L1 were two methylated products which were obtained after hydrolysis of the ester. The major metabolites of euphorbetin L2,euphorbetin L8 and 6( 17),12( E)-lathyrol-5,15-diacetate-3-phenylacetate were hydrolysis products of the ester. Conclusion: The main metabolic pathway of euphorbetin L1 is methylation and hydrolysis of the ester. The main metabolic pathway of euphorbetin L2,euphorbetin L8 and 6( 17),12( E)-lathyrol-5,15-diacetate-3-phenylacetate is hydrolysis of the ester. LC/MS/MS can identify the metabolites of euphorbetin L1,euphorbetin L2,euphorbetin L8 and 6( 17),12( E)-lathyrol-5,15-diacetate-3-phenylacetate in Caco-2 cells quickly and sensitively.

Combinational Treatment of Curcumin and Quercetin against Gastric Cancer MGC-803 Cells in Vitro.

Gastric cancer remains a major health problem worldwide. Natural products, with stronger antitumor activity and fewer side effects, are potential candidates for pharmaceutical development as anticancer agents. In this study, quercetin and curcumin were chosen for testing and were applied separately and in combination to human gastric cancer MGC-803 cells. The MTT assay was used to evaluate cell growth inhibition. Annexin V-FITC/PI was carried out to measure apoptosis rate. Flow cytometry was performed to analyze mitochondrial membrane potential levels. Western blots were applied to detect expression of cytochrome c, total and phosphorylated ERK and AKT. Combined treatment with curcumin and quercetin resulted in significant inhibition of cell proliferation, accompanied by loss of mitochondrial membrane potential (ΔΨm), release of cytochrome c and decreased phosphorylation of AKT and ERK. These results indicate that the combination of curcumin and quercetin induces apoptosis through the mitochondrial pathway. Notably, effect of combined treatment with curcumin and quercetin on gastric cancer MGC-803 cells is stronger than that of individual treatment, indicating that curcumin and quercetin combinations have potential as anti-gastric cancer drugs for further development.

[Metabolites Identification for Alkaloids from Nelumbinis Plumula in Caco-2 Cells by LC/MS/MS].

OBJECTIVE: To identify the metabolites of norcoclaurine,liensinine, isoliensinine and neferine in Caco-2 cells by LC/ MS/MS. METHODS: After Caco-2 cells were treated with norcoclaurine, liensinine, isoliensinine or neferine for 3, 6 and 12 h, samples were collected, purified and then analyzed by LC/MS/MS. The structures of the metabolites were elucidated by molecular masses, retention times, MS and MS/MS spectra comparing with those of the parent drug. RESULTS: The procedure identified that the major metabolites of norcoclaurine were methylnorcoclaurine and norcoclaurine-glucuronide, the major metabolite of liensinine was demethyl-liensinine, the major metabolite of isoliensinine was demethyl-isoliensinine, the major metabolites of neferine were liensinine, isoliensinine and their further demethylation products. CONCLUSION: LC/MS/MS is simple, rapid and sensitive for the metabolites identification. Methylation, demethylation and glucuronidation are main metabolic pathways of alkaloids from Nelumbinis Plumula in Caco-2 cells.

Trends of injury mortality during the COVID-19 period in Guangdong, China: a population-based retrospective analysis.

OBJECTIVE: We aimed to ascertain the trends of injury mortality during the COVID-19 period in southern China. METHODS: We conducted a population-based retrospective analysis to compare the mortality changes of all-cause injury and transport injuries, poisoning, falls, fire/heat/hot substances, drowning, self-harm and interpersonal violence, which were further stratified by sex and age. Comparisons were made between the COVID-19 period (between January 2020 and June 2020) and control period (between January 2019 and June 2019) in Guangdong province. We used the negative binomial models to explore the associations of deaths during the COVID-19 period, according to the different sex and age strata. RESULTS: The all-cause injury mortality in Guangdong province decreased significantly from 28.65 per 100 000 population during the control period to 23.24 per 100 000 population during COVID-19 pandemic period. Similar results were found in specific injury categories. Mortality of self-harm increased by 139.26% in the 10-14 year group during the COVID-19 period as compared with the control period. Although mortality changes in some groups were not statistically significant, some increases were noteworthy during the COVID-19 period (ie, self-harm, transport injury and falls) in the 70-79 year group. The corresponding increase in mortality rate was 16.83%, 3.32% and 4.92%, respectively. CONCLUSION: The mortality of all-cause injury, transport injury and drowning during the COVID-19 pandemic was consistently decreased. However, the increase in mortality associated with falls, fire/heat/hot substance injury and self-harm in specific age populations warrant the targeted control and prevention measures for the population at risk.

Jian-Pi-Yi-Fei granule suppresses airway inflammation in mice induced by cigarette smoke condensate and lipopolysaccharide.

INTRODUCTION: As a chronic, progressive, and lethal pulmonary disease, chronic obstructive pulmonary disease (COPD) is lacking effective treatment. Chronic inflammatory processes, including inflammatory cytokines, play an important role with in its pathogenesis. Jianpiyifei (JPYF) granule is a traditional Chinese herbal formula historically used to strengthen the spleen and tonify the lung. JPYF is used clinically to treat stable COPD. However, whether the purported anti-inflammatory effect of JPYF in COPD involves regulation of key inflammatory cytokines is not clear. MATERIALS AND METHODS: The mice model of pulmonary inflammation was induced by lipopolysaccharide (LPS) and cigarette smoke condensate (CSC). The influence of JPYF on airway inflammation in vivo was investigated. Mice were divided into three groups: control, model, and treatment groups. In the CSC + LPS model group and JPYF treatment group, intratracheal injection of CSC and LPS was used to induce airway inflammation for 5 days. JPYF group animals were also orally administered 5.5 g/kg JPYF granule for 12 days. RESULTS: The number of neutrophils and total cells in bronchoalveolar lavage fluid of the JPYF group were markedly lower than in the model group. The levels of interleukin (IL)-1 ß and IL-6 were lower; tumor necrosis factor-alpha was downregulated, and IL-10 was higher in the JPYF group than the model group. In the JPYF group, histone deacetylase 2 (HDAC2) activity and protein expression were restored. CONCLUSION: The anti-inflammatory activity of JPYF involves the suppression of pro-inflammatory cytokines, enhanced IL-10 secretion, and the restoration of HDAC2 activity.

Bruceine D induces apoptosis in human chronic myeloid leukemia K562 cells via mitochondrial pathway.

Chronic myeloid leukemia (CML), an acquired malignant myeloproliferative disorder of hematopoietic stem cells, is one of the three most common forms of leukemia. In this study, we investigated the effects of bruceine D, which have been isolated from Brucea javanica (L.) Merr. on human chronic myeloid leukemia K562 cells. MTT assay was used to evaluate cell growth inhibition. Flow cytometry was performed to analyze mitochondrial membrane potential (ΔΨm). Western blot was applied to detect expression of cytochrome c, caspases-9, -3, PARP and other proteins. Bruceine D exhibited potent cytotoxicity to K562 cells with IC50 of 6.37 ± 0.39 µM. It led to loss of ΔΨm, release of cytochrome c, activation of caspases-9, -3 and cleavage of PARP, which suggested that bruceine D induced apoptosis of K562 cells through mitochondrial pathway. In addition, bruceine D inhibited the phosphorylation of AKT and ERK. It's indicative that the potent anticancer activity of bruceine D be related to MAPK and PI3K pathways.