Efficacy and safety of omega-3 fatty acids on liver-related outcomes in patients with nonalcoholic fatty liver disease: A protocol for a systematic review and meta-analysis.

BACKGROUND: Non-alcoholic fatty liver disease (NAFLD), especially non-alcoholic steatohepatitis, which is considered as the hepatic manifestation of metabolic syndrome, has a great prevalence all over the world. New drugs are urgently needed for the treatment of NAFLD. This review will be to assess the efficacy and safety of omega-3 polyunsaturated fatty acids (n-3 PUFAs) on liver-related outcomes (liver histology and liver enzymes) in patients with NAFLD. METHODS: We will search 5 databases for relative studies: Medline, the Cochrane Library, EMBASE, Web of Science, and ClinicalTrials.gov and identified all reports of randomized controlled trials published prior to July 2020. Two authors will independently scan the articles searched, extract the data from articles included, and assess the risk of bias by Cochrane tool of risk of bias. Disagreements will be resolved by discussion among authors. All analysis will be performed based on the Cochrane Handbook for Systematic Reviews of Interventions. Fixed-effects model or random-effects model will be used to calculate pooled estimates of weighted mean difference with 95% confidence intervals. RESULTS: This systematic review aims to examine the effect of n-3 PUFAs on liver histology and liver enzymes in patients with NAFLD. CONCLUSIONS: These findings will provide guidance to clinicians and patients on the use of n-3 PUFAs for NAFLD. ETHICS AND DISSEMINATION: This study is a protocol for a systematic review of n-3 PUFAs as a treatment of NAFLD patients. This review will be published in a journal and disseminated in print by peer-review. SYSTEMATIC REVIEW REGISTRATION: INPLASY202050008.

[Paeonol inhibits macrophage M1 polarization by down-regulating miR-155/JAK1-STAT1 pathway].

The aim of this paper was to investigate the effect and mechanism of paeonol on peritoneal macrophage M1 polarization in mice, explore whether the intervention action is related to the down-regulation of miR-155 and the inhibition of downstream JAK1-STAT1 pathway, and provide a new idea for the molecular mechanism of paeonol against atherosclerosis(AS). Lipopolysaccharide(LPS) and interferon-γ(IFN-γ) were used to stimulate macrophages for 24 hours to establish the M1 polarization model, and paeonol was given 24 hours before co-stimulation to provide a pre-protective effect on cells. CCK-8 assay was used to detect the cells damage induced by LPS and IFN-γ co-stimulation; flow cytometry was used to detect the expression of M1 surface markers F4/80 and CD86. ELISA was used to detect the secretion of interleukin 6(IL-6) and tumor necrosis factor-α(TNF-α) in supernatant. RT-qPCR was used to detect the expression of miR-155, and Western blot was used to detect the protein expression at JAK1-STAT1-SOCS1 pathway. The results showed that LPS and IFN-γ had no obvious damage to the cells at the optimal concentration, but they induced macrophages polarized to M1, resulted in high expression of M1 type marker factors F4/80 and CD86 on the cell surface, and increased secretion of IL-6 and TNF-α on the cell surface(P<0.05 or P<0.01). Paeonol significantly reduced the LPS and IFN-γ-induced high expression of F4/80 and CD86, the secretion of inflammatory factors IL-6 and TNF-α(P<0.05 or P<0.01), decreased the expression level of miR-155, significantly down-regulated the protein phosphorylation level of JAK1-STAT1 and up-regulated the protein expression of SOCS1(P<0.01) in RAW264.7 cells. The results showed that paeonol could inhibit M1 polarization of macrophages by down-regulating cell surface marker factors and inflammatory factors secreted by cells, which may be related to the down-regulation of miR-155 expression and the inhibition JAK1-STAT1 pathway activation.

Effects of vitamin D supplementation on serum lipid profile in women with polycystic ovary syndrome: A protocol for a systematic review and meta-analysis.

BACKGROUND: Polycystic ovary syndrome (PCOS) is the commonest endocrine disorder in reproductive-aged women. In addition to the reproductive consequences, PCOS is also characterized by a metabolic disorder, which may play a part in the etiology of anovulation and has important implications for long-term health as well. Vitamin D deficiency is prevalent in PCOS and there is a close relationship between metabolic dysfunction and vitamin D status in women with PCOS. The purpose of this systematic analysis is to evaluate the effect of vitamin D supplementation on serum lipid profiles in patients with PCOS. METHODS: We will search five databases for relative studies: Medline, the Cochrane Library, EMBASE, Web of Science, and ClinicalTrials.gov and identified all reports of randomized controlled trials published prior to July 2020. Two authors will independently scan the articles searched, extract the data from articles included, and assess the risk of bias by Cochrane tool of risk of bias. Disagreements will be resolved by discussion among authors. All analysis will be performed based on the Cochrane Handbook for Systematic Reviews of Interventions. Fixed-effects model or random-effects model was used to calculate pooled estimates of weighted mean difference (WMD) with 95% confidence intervals. RESULTS: This review will be to assess the effect of vitamin D supplementation on serum lipid profiles in patients with PCOS. The results of the study will be published in a scientific journal after peer-review. CONCLUSIONS: These findings will provide guidance to clinicians and patients on the use of vitamin D for PCOS with dyslipidemia. ETHICS AND DISSEMINATION: This study is a protocol for a systematic review of vitamin D as a treatment of dyslipidemia in PCOS patients. SYSTEMATIC REVIEW REGISTRATION: INPLASY202050007.

[Prosapogenin A inhibits cell growth of MCF7 via downregulating STAT3 and glycometabolism-related gene].

This study is to investigate the inhibitory effect and mechanism of prosapogenin A (PSA) on MCF7. MTT assay was performed to determine the inhibitory effect of PSA on MCF7 cells. PI/Hoechst 33342 double staining was used to detect cell apoptosis. RT-PCR was used to test the mRNA levels of STAT3, GLUT1, HK and PFKL. Western blotting was performed to determine the expression of STAT3 and pSTAT3 protein in MCF7 cells. The results showed that PSA could dose-dependently inhibit cell growth of MCF7 followed by IC50 of 9.65 micrmol x L(-1) and promote cell apoptosis of MCF7. Reduced mRNA levels of STAT3, HK and PFKL were observed in MCF7 cells treated with 5 micromol x L(-1) of PSA. PSA also decreased the level of pSTAT3 protein. STAT3 siRNA caused decrease of mRNA of GLUT1, HK and PFKL which indicated STAT3 could regulate the expressions of GLUT1, HK and PFKL. The results suggested that PSA could inhibit cell growth and promote cell apoptosis of MCF7 via inhibition of STAT3 and glycometabolism-related gene.

Prosapogenin A induces apoptosis in human cancer cells in vitro via inhibition of the STAT3 signaling pathway and glycolysis.

Signal transducer and activator of transcription 3 (STAT3) is considered to be an oncogene. Blocking STAT3 signaling may induce growth arrest and apoptosis in different types of tumors. Cancer cells utilize the glycolytic pathway to maintain cell growth even when adequate oxygen is present. Glycolysis inhibition is a potential therapeutic modality. In the present study, the effects of Prosapogenin A (PSA) from the traditional Chinese medicine, Veratrum, on apoptosis, the STAT3 signaling pathway and glycometabolism in cancer cells were investigated. The results indicated that PSA induced growth inhibition and apoptosis in HeLa, HepG2 and MCF-7 cells. PSA inhibited the STAT3 signaling pathway and modulated the expression of glycometabolism-related genes. The results indicate that the inhibition of the STAT3 signaling and glycometabolism pathways contributes to the PSA-mediated apoptosis of HeLa, HepG2 and MCF-7 cells.

[Impact of S100P expression on clinical outcomes of gastric cancer patients with adjuvant chemotherapy of oxaliplatin and its mechanisms].

OBJECTIVE: To investigate the impact of the expression of S100P on the prognosis and tumor chemosensitivity in patients with resectable gastric cancer and its mechanisms. METHODS: The expression of S100P was analyzed in 121 resected primary gastric cancer tissues by using tissue array of immunohistochemistry excised from January 2003 to December 2007. The patients received adjuvant chemotherapy with oxaliplatin. The pEGFP-S100P plasmid was constructed and was transfected into BGC823 cell line to establish gastric cancer cell line with over-expression of human S100P, BGC823-S100P. The expression level of S100P was determined by real-time PCR and Western blot assay. The chemosensitivity of BGC823-S100P cell line to oxaliplatin was detected by 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium (MTT) assay. RESULTS: The S100P was positively expressed in 64 tumors (52.9%, 64/121). Although there was no significant relation between the expression of S100P and tumor T staging (P = 0.683), N staging (P = 0.472), M staging (P = 0.770) and differentiation (P = 0.553), Wilcoxon test showed that the 5-year cumulative survival rate of patients with positive S100P expression was significantly higher than that of patients with negative expression (20.3% vs. 3.5%, P = 0.034). Furthermore, overexpressed of S100P was found in the BGC823 cell line, BGC823-S100P. The mRNA and protein level of S100P in pEGFP transfected BGC823-S100P cell lines were significantly higher than those in control group (8.42 ± 1.38 vs. 0.83 ± 0.11 and 3.52 ± 0.48 vs. 0.97 ± 0.19, all P < 0.05). It indicated with MTT assay that the half-inhibitory concentration (IC(50)) to oxaliplatin decreased in BGC823-S100P cells, and was significantly lower than that in vector-only transfected cells [(142 ± 16) mg/L vs. (266 ± 11) mg/L, P = 0.032]. CONCLUSIONS: S100P may also be a potentially novel independent prognostic factor in gastric cancer patients following curative resection. And it could improve the cumulative survival of the patients through enhancing the chemosensitivity of tumor cell line to oxaliplatin.

[Effects of biodiesel on fine particles (PM2.5) and polycyclic aromatic hydrocarbons from diesel engine].

PM2.5 emissions and polycyclic aromatic hydrocarbons (PAHs) in PM2.5 of pure biodiesel derived from different feedstocks were investigated and compared with diesel fuel. B100-1 (soyabean oil derived), B100-2 (waste oil derived) and diesel fuel were tested on a diesel engine bench at four operating conditions, including two steady speeds of different loads. The fine particles were collected by fiber quartz filter and particle phase PAHs were analyzed by GC-MS. Compared with diesel fuel, biodiesel decreased PM2.5 emission rates with a maximal reduction rate of 37.3% at operating modes of high loads, while increased PM2.5 emission rates at low loads. PAHs emission rates from biodiesel decreased at all tested modes, with a maximal reduction rate of 77.6%. The emission rates of PM2.5 and PAHs of B100-2 were 14.7% and 17.8% times of B100-1. Low molecular weight PAHs dominated in the emission of three fuels with phenanthrene as maxima and 2-ring and 3-ring PAHs accounted for more than 50% of the total PAHs. Toxic equivalence of PAHs emissions of biodiesel was decreased greatly compared with that of diesel.

Evaluation of hyperbaric oxygen treatment of neuropsychiatric disorders following traumatic brain injury.

BACKGROUND: Improvement of clinical symptoms following hyperbaric oxygen (HBO) treatment of neuropsychiatric disorders arising from traumatic brain injury was proved by our previous study. This study was aim to obtain the evidence of other changes. METHODS: Three hundred and ten patients with neuropsychiatric disorders arising from traumatic brain injury were treated twice with hyperbaric oxygen. Cerebral single photon emissions computed tomography (SPECT) images and computed tomography scans (CT) before and after hyperbaric oxygen treatment, were compared. RESULTS: Before treatment, the proportion of abnormal cerebral changes detected by SPECT was 81.3% but only 15.2% by CT. After HBO treatment, 70.3% of SPECT scans showed no abnormalities and these patients were clinically improved. Treatment improved regional cerebral blood flow. CONCLUSION: SPECT was much more sensitive than CT in the diagnosis of neuropsychiatric disorders following hyperbaric oxygen treatment of neuropsychiatric disorders arising from traumatic brain injury.

Elimination of formaldehyde over Cu-Al2O3 catalyst at room temperature.

Catalytic elimination of formaldehyde (HCHO) was investigated over Cu-Al2O3 catalyst at room temperature. The results indicated that no oxidation of HCHO into CO2 occurs at room temperature, but the adsorption of HCHO occurs on the catalyst surface. With the increase of gas hourly space velocity (GHSV) and inlet HCHO concentration, the time to reach saturation was shortened proportionally. The results of the in situ DRIFTS, Density functional theory calculations and temperature programmed desorption(TPD) showed that HCHO was completely oxidized into HCOOH over Cu-Al2O3 at room temperature. With increasing the temperature in a flow of helium, HCOOH was completely decomposed into CO2 over the catalyst surface, and the deactivated Cu-Al2O3 is regenerated at the same time. In addition, although Cu had no obvious influence on the adsorption of HCHO on Al2O3, Cu dramatically lowered the decomposition temperature of HCOOH into CO2. It was shown that Cu-Al2O3 catalyst had a good ability for the removal of HCHO, and appeared to be promising for its application in destroying HCHO at room temperature.

Cerebral perfusion SPECT imaging for assessment of the effect of hyperbaric oxygen therapy on patients with postbrain injury neural status.

OBJECTIVE: To evaluate the effects of hyperbaric oxygen (HBO) therapy on patients with postbrain injury neural status. METHODS: Two to 4 courses of HBO therapy and/or medications were used to treat 320 patients who were randomly divided into two groups. Assessment was made with (99m)Tc-ethyl cysteinate dimer ( (99m)Tc-ECD) single photon emission computed tomography (SPECT) before and after treatment. RESULTS: There was a significant difference between the HBO therapy group and the non-HBO therapy group. HBO therapy was superior to medication treatment alone in the recovery of clinical symptoms, control of epilepsy, and resolution of hydrocephalus (P<0.01). CONCLUSIONS: HBO therapy has specific curative effects on patients with postbrain injury neural status, and (99m)Tc-ECD SPECT could play an important role in diagnosing postbrain injury neural status and monitoring the therapeutic effects of HBO.