New insights into changes in phosphorus profile at sediment-water interface by microplastics: Role of benthic bioturbation.

Microplastics (MPs) have attracted increasing attention due to their ubiquitous occurrence in freshwater sediments and the detrimental effects on benthic invertebrates. However, a clear understanding of their downstream impacts on ecosystem services is still lacking. This study examines the effects of bio-based polylactic acid (PLA), fuel-based polyethylene terephthalate (PET), and biofilm-covered PET (BPET) MPs on the bioturbator chironomid larvae (Tanypus chinensis), and the influence on phosphorus (P) profiles in microcosms. The changes in biochemical responses and metabolic pathways indicated that MPs disrupted energy synthesis by causing intestinal blockage and oxidative stress in T. chinensis, leading to energy depletion and impaired bioturbation activity. The impairment further resulted in enhanced sedimentary P immobilization. For larval treatments, the internal-P loadings were respectively 11.4%, 8.6%, and 9.0% higher in the PLA, PET, and BPET groups compared to the non-MP control. Furthermore, the influence of bioturbation on P profiles was MP-type dependent. Both BPET and PLA treatments displayed more obvious impacts on P profiles compared to PET due to the changes in MP bioavailability or sediment microenvironment. This study connects individual physiological responses to broader ecosystem services, showing that MPs alter P biogeochemical processes by disrupting the bioturbation activities of chironomid larvae.

Methylene Blue Reduces Retinal Cell Inflammation, Apoptosis, and Oxidative Stress in a Rat Model of Diabetic Retinopathy via Sirtuin 1 Activation.

Objective: Diabetic retinopathy (DR), characterized by neuronal damage in the retina, is primarily driven by oxidative stress resulting from diabetes (DM). This study investigated the potential effects of methylene blue (MB) on streptozotocin (STZ)-induced DR. Methods: A rat model of DR was established via STZ injection, while a cell model was created using high-glucose (HG) exposure of human retinal microvascular endothelial cells. Evaluation of oxidative stress markers, pro-inflammatory cytokines, and pro-apoptotic proteins was performed based on their expression profiles in human retinal microvascular endothelial cells. Results: MB treatment significantly upregulated the expression of sirtuin 1 (SIRT1), which was found to be downregulated in the retinal tissues of STZ-treated rats and HG-exposed human retinal microvascular endothelial cells, as determined by polymerase chain reaction (PCR). Furthermore, MB therapy effectively suppressed STZ-induced oxidative stress, inflammation, and cell death. Consistent with the in vivo findings, MB activated the expression of SIRT1, thereby protecting HG-treated human retinal microvascular endothelial cells against oxidative stress, inflammation, and apoptosis. Conclusion: These results support the conclusion that MB mitigates DR by activating SIRT1, leading to a reduction of inflammation, apoptosis, and oxidative stress.

Biomarker Identification of Maternal Genistein Exposure Induced Obesity by Metabonomics Analysis.

The objective of this study was to confirm the effect of maternal genistein exposure on body weight of male offspring and the metabolic alterations associated with maternal genistein-induced obesity. Pregnant female Sprague-Dawley (SD) rats were supplemented with 300 mg/kg diet of genistein (GEN) or no genistein (CON) throughout pregnancy and lactation. The growth of male offspring was investigated until 12 week age and the mechanism of obesity was studied using metabonomics by ultra performance liquid chromatography and quadrupole time-of-flight (UPLC Q-TOF) MS with electrospray ionization in positive ESI mode (ESI+). Compared with the CON group, body weight, fat pad and food intake of male offspring in GEN group were increased significantly at the age of weeks 10 to 12 (p<0.05). Ten urine principal metabolites contributing to the clusters were identified, including increased 8-Isoprostaglandin F2a, and decreased L-Proline, Betaine, L-Acetylcarnitine, Norsalsolinol, Indoleacrylic acid, L-Tryptophan, Lysophosphatidylcholines (LysoPC) (20 : 4), Lysophosphatidylethanolamines (LysoPE) (18 : 1) and LysoPC (O-18 : 0). Our results confirmed weight-increasing effects of maternal genistein exposure, accompanied by favorable changes in metabolites in the male offspring' urine. Therefore, this research enables us to better understand obesity and predict risk of obesity-related disease by studying metabolites present in the urine.

Effects of Long-Term In Vivo Exposure to Di-2-Ethylhexylphthalate on Thyroid Hormones and the TSH/TSHR Signaling Pathways in Wistar Rats.

Di-(2-ethylhexyl)phthalate (DEHP) was a widely used chemical with human toxicity. Recent in vivo and in vitro studies suggested that DEHP-exposure may be associated with altered serum thyroid hormones (THs) levels, but the underlying molecular mechanisms were largely unknown. To explore the possible molecular mechanisms, 128 Wistar rats were dosed with DEHP by gavage at 0, 150, 300, and 600 mg/kg/day for 3 months (M) and 6 M, respectively. After exposure, expression of genes and proteins in the thyroid, pituitary, and hypothalamus tissues of rats were analyzed by Q-PCR and western blot, while the sera and urine samples were assayed by radioimmunoassay and ELISA. Results showed that serum THs levels were suppressed by DEHP on the whole. DEHP treatment influenced the levels of rats' thyrotropin releasing hormone receptor (TRHr), Deiodinases 1 (D1), thyroid stimulating hormone beta (TSHß), sodium iodide symporter (NIS), thyroid stimulating hormone receptor (TSHr), thyroperoxidase (TPO), thyroid transcription factor 1 (TTF-1), and thyroglobulin (TG) mRNA/protein expression in the hypothalamus-pituitary-thyroid (HPT) axis and decreased urine iodine. Taken together, observed findings indicate that DEHP could reduce thyroid hormones via disturbing the HPT axis, and the activated TSH/TSHR pathway is required to regulate thyroid function via altering TRHr, TSHß, NIS, TSHr, TPO, TTF-1 and TG mRNA/protein expression of the HPT axis.

Soy Protein Supplementation Reduces Clinical Indices in Type 2 Diabetes and Metabolic Syndrome.

PURPOSE: Clinical trials have studied the use of soy protein for treating type 2 diabetes (T2D) and metabolic syndrome (MS). The purpose of this study was to outline evidence on the effects of soy protein supplementation on clinical indices in T2D and MS subjects by performing a meta-analysis of randomized controlled trials (RCTs). MATERIALS AND METHODS: We searched PubMed, EMBASE, and Cochrane databases up to March 2015 for RCTs. Pooled estimates and 95% confidence intervals (CIs) were calculated by the fixed-and-random-effects model. A total of eleven studies with eleven clinical variables met the inclusion criteria. RESULTS: The meta-analysis showed that fasting plasma glucose (FPG) [weighted mean difference (WMD), -0.207; 95% CI, -0.374 to -0.040; p=0.015], fasting serum insulin (FSI) (WMD, -0.292; 95% CI, -0.496 to -0.088; p=0.005), homeostasis model of assessment for insulin resistance index (HOMA-IR) (WMD, -0.346; 95% CI, -0.570 to -0.123; p=0.002), diastolic blood pressure (DBP) (WMD, -0.230; 95% CI, -0.441 to -0.019; p=0.033), low-density lipoprotein cholesterol (LDL-C) (WMD, -0.304; 95% CI, -0.461 to -0.148; p=0.000), total cholesterol (TC) (WMD, -0.386; 95% CI, -0.548 to -0.225; p=0.000), and C-reactive protein (CRP) (WMD, -0.510; 95% CI, -0.722 to -0.299; p=0.000) are significant reduced with soy protein supplementation, compared with a placebo control group, in T2D and MS patients. Furthermore, soy protein supplementation for longer duration (≥6 mo) significantly reduced FPG, LDL-C, and CRP, while that for a shorter duration (<6 mo) significantly reduced FSI and HOMA-IR. CONCLUSION: Soy protein supplementation could be beneficial for FPG, FSI, HOMA-IR, DBP, LDL-C, TC, and CRP control in plasma.

Calcium supplementation increases circulating cholesterol by reducing its catabolism via GPER and TRPC1-dependent pathway in estrogen deficient women.

BACKGROUND: Limited studies have addressed the effects of calcium supplementation (CaS) on serum total cholesterol (TC) in postmenopausal women and the results are inconclusive. Moreover, the potential mechanisms through which CaS regulates cholesterol metabolism in the absence of estrogen are still sealed for the limitation of human being study. METHODS: Cross-sectional survey, animal and in vitro experiments were conducted to investigate the effect of CaS on endogenous cholesterol metabolism in estrogen deficiency and identify its potential mechanisms. Ovariectomized rats were used to mimic estrogen deficiency. In vitro, HepG2 cell line was exposed to estradiol and/or calcium treatment. RESULTS: We demonstrated that CaS significantly increased serum TC and the risk of hypercholesterolemia and myocardial infarction in postmenopausal women. Increased serum TC in estrogen deficiency was caused mainly by decreased cholesterol catabolism rather than increased synthesis. This was mediated by reduced 7α-hydroxylase resulting from increased liver intracellular Ca(2+) concentrations, reduced intracellular basal cAMP and subsequent up-regulation of SREBP-1c and SHP expression. Estrogen had a protective role in preventing CaS-induced TC increase by activating the G-protein coupled estrogen receptor, which mediated the estrogen effect through the transient receptor potential canonical 1 cation channel. CONCLUSIONS: CaS increases endogenous serum TC via decreasing hepatic cholesterol catabolism in estrogen deficiency. G-protein coupled estrogen receptor is shown to be a key target in mediating CaS-induced TC increase. CaS should be monitored for the prevention of serum TC increase during menopause.

Soy isoflavone supplementation could reduce body weight and improve glucose metabolism in non-Asian postmenopausal women--a meta-analysis.

OBJECTIVE: The objective of this study was to conduct a systematic review and a meta-analysis to confirm the effects of soy isoflavone supplementation on body weight, fasting glucose, and insulin level in non-Asian postmenopausal women. METHODS: We searched the PubMed, EMBASE, and Cochrane databases up to October 2010 for randomized controlled trials regarding the effects of isoflavone supplementation on body weight, fasting glucose, and insulin level. Pooled estimates and 95% confidence intervals (CIs) were calculated by the fixed-and-random-effects model. RESULTS: Nine studies with 528 participants for body weight, 11 studies with 1182 participants for fasting glucose, and 11 studies with 1142 participants for fasting insulin were included, respectively. Significant reductions were found in body weight [weighted mean difference (WMD), -0.515; 95%CI: -0.895 to -0.134; P = 0.008), glucose level (WMD, -0.189; 95%CI: -0.344 to -0.033), and fasting insulin level (WMD, -0.940; 95%CI: -1.721 to -0.159) with soy isoflavone supplementation compared with placebo control group in non-Asian postmenopausal women after adjusted by unpublished studies. Furthermore, isoflavone supplementation in shorter duration (<6 mo) could significantly reduce body weight (WMD, -0.506; 95%CI: -0.888 to -0.124; P = 0.009) and longer duration (≥ 6 mo) could significantly reduce blood glucose in postmenopausal women (WMD, -0.270; 95%CI: -0.430 to -0.110; P = 0.001). Meanwhile, more reduction in body weight was observed in the lower dose subgroup (dose < 100 mg). Moreover, it is more effective to reduce body weight and fasting insulin level with soy isoflavone supplementation in normal weight (body mass index < 30) than obese (body mass index ≥ 30) women. CONCLUSIONS: This meta-analysis showed soy isoflavone supplementation could be beneficial for body weight reduction, glucose, and insulin control in plasma. Large and well-designed studies are recommended to confirm this conclusion.

[Clinical observation on acupoint injection therapy for chronic gastritis of gastric blood stasis type].

OBJECTIVE: To objectively evaluate the clinical effect of acupoint injection therapy for chronic gastritis of gastric blood stasis type. METHODS: One hundred and two cases arranged by registration order were randomly divided into an acupoint injection group and a medicine group, 51 cases in each group. The acupoint injection group was treated with acupoint injection of compound Danshen injection, and Zusanli (ST 36) and Weishu (BL 21) were selected, and the medicine group with oral administration of Omeprazole. After 2 weeks of treatment, the clinical effect and improvement of endoscopic gastric mucosal lesions were observed. RESULTS: The clinical total effective rate of 96.1% (49/51) in the acupoint injection group was better than 76.5% (39/51) in the medicine group (P < 0.01). The symptom score decreased significantly after treatment and the gastric mucosal lesion was significantly improved in both of the two groups (all P < 0.05), and the acupoint injection group was superior to the medicine group (all P < 0.05). CONCLUSION: Acupoint injection has outstanding effect for treatment of chronic gastritis of gastric blood stasis type and this therapy is worth generalizing and applying.

Soy isoflavone and its effect to regulate hypothalamus and peripheral orexigenic gene expression in ovariectomized rats fed on a high-fat diet.

OBJECTIVE: To explore the effect of soy isoflavone on obesity in the light of hypothalamus and peripheral orexigenic gene regulation. METHODS: Fifty-four female rats were randomly assigned to 6 groups: one sham-operated group (SHAM), one ovariectomized (OVX) control group, three OVX groups fed with 400 ppm (L-SI), 1200 ppm (M-SI) and 3600 ppm (H-SI) isoflavone respectively, and one OVX group receiving 0.45 ppm diethylstilbestrol (EC). All rats were allowed to take high-fat diet for 4 weeks. Some neuropeptides were measured by RT-PCR. These neuropeptides included NPY, pro-opiomelanocortin (POMC), cocaine and amphetamine regulated transcript (CART), orexin, melanin-concentrating hormone (MCH), melanin-concentrating hormone precursor (P-MCH), ghrelin, and leptin. RESULTS: Compared with the OVX control group, the body weight and food intake in the H-SI group were reduced significantly and there was a significant dose-dependent manner in the 3 isoflavone groups. The results of RT-PCR showed that the NPY level in the 3 isoflavone groups was significantly increased and the POMC/CART gene expression decreased significantly in rats' hypothalamus compared with that in the OVX control group. However, the expression of orexin, MCH and P-MCH had no change. The peripheral grelin mRNA expression was higher in the 3 isoflavone groups, while leptin gene expression in the fat was not consistent. CONCLUSIONS: This research showed that isoflavone could prevent obesity induced by high-fat diet and ovariectomy through regulating hypothalamus and peripheral orexigenic gene expressions associated with food intake.