Effects of natural dihydrochalcones in sweet tea (Lithocarpus polystachyus) on diabetes: a systematical review and meta-analysis of animal studies.

Sweet tea (Lithocarpus polystachyus Rehd.), a natural functional food highly rich in dihydrochalcones including trilobatin, phlorizin and phloretin, is reported to possess numerous biological activities especially for treating diabetes. Here, the aim of this systematical review and meta-analysis is to assess the effect of dihydrochalcones in sweet tea (DST) on diabetes and summarize their possible mechanisms. We searched in eight databases including Embase, PubMed, Cochrane, Web of Science, WanFang database, VIP database, China National Knowledge Infrastructure and China Biology Medicine from Jan 2000 to Nov 2021 and ultimately included 21 animal studies in this review. A total of 10 outcome measurements including blood lipid indexes, blood glucose, insulin resistance indicators and oxidative stress biomarkers were extracted for meta-analysis using RevMan 5.4 software. DST significantly decreased the levels of triglyceride (TG), total cholesterol (TC), low-density lipoprotein cholesterol (LDL-c), blood glucose (BG), homeostasis model assessment of insulin resistance (HOMA-IR) and malondialdehyde (MDA), and increased high-density lipoprotein cholesterol (HDL-c), superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activity in diabetic animal models. In summary, DST could treat diabetes by regulation of blood glucose/lipid metabolism, oxidative/carbonyl stress, inflammatory response etc.

[Treatment of Petrochemical Treatment Plant Secondary Effluent by Fenton Oxidation].

Fenton oxidation was applied to treat the petrochemical treatment plant secondary effluent by the continuous flow configuration. The effect of Fenton agent dosage on the COD and phosphorus removal and the variation of the dissolved organic matter characteristics during the treatment process were investigated. The results showed the average COD and PO(4)3- -P concentrations were 64.8 mg.L-1 and 0. 79 mg.L-1, respectively. When the dosage of H2O (30%), FeSO4.7H2O and PAM were 0. 4 mL.L-1, 0. 8 mg.L-1 and 0. 9 mg.L-1 and the residence time was 30 min, the average removal rate of COD and PO(4)3- -P were 24. 3% and 95. 5% respectively. The effluent COD was lower than 50 mg.L-1. The percentage of dissolved organic matters with molecular weight less than 1 x 10(3) was 80. 4% in the raw wastewater, however, the percentage increased to 95. 6% when treated by Fenton oxidation. Three-dimensional fluorescence analysis showed that the Fenton oxidation can effectively remove protein and phenols. GC-MS results showed that there were about 117 kinds of organic matters detected in the secondary effluent, while the number reduced to 27 after oxidation by Fenton. The organics containing unsaturated bond had a better removal than those of other types of organics. Fenton oxidation can be used in the advanced treatment of petrochemical secondary effluent.

Telomerase activity and telomerase reverse transcriptase expression induced by selenium in rat hepatocytes.

OBJECTIVE: To investigate the effects of sodium selenite on telomerase activity, apoptosis and expression of TERT, c-myc and p53 in rat hepatocytes. METHODS: Selenium at doses of 2.5, 5.0, and 10 micromol/kg was given to SD rats by gavage. In rat hepatocytes, telomerase activity was measured by the telomeric repeat amplification protocol (TRAP), apoptosis was detected by flow cytometry, and expressions of telomerase reverse transcriptase (TERT), c-myc and p53 were analyzed by reverse transcription-polymerase chain reaction (RT-PCR). c-Myc and P53 proteins were detected by immunochemistry. RESULTS: Selenium at doses of 2.5, 5.0, and 10 micromol/kg significantly increased hepatocellular telomerase activity and induced apoptosis in a dose-dependent manner. Although selenium at doses of 2.5, 5.0, and 10 micromol/kg displayed no obvious enhancing effect on the TERT mRNA expression in rat hepatocytes (P > 0.05), it significantly increased the c-myc mRNA and p53 mRNA expression at the dose of 10 micromol/kg (P < 0.05). Selenium at doses of 5.0 and 10 micromol/kg obviously increased the content of P53 protein in rat hepatocytes, but only at the dose of 10 micromol/kg, it significantly promoted the value of c-Myc protein in them. CONCLUSION: Selenium can slightly increase telomerase activity and TERT expression, and significantly induce apoptosis and over-expression of c-myc and p53 at relatively high doses. The beneficial effects of selenium on senescence and aging may be mediated by telomerase activation and expression of TERT, c-myc, and p53 in rat hepatocytes.

[Effects of earthworm (Eisennia foetida ) on As, P uptake by maize and As, P fractional transformation in the rhizosphere].

A pot experiment was conducted to examine the roles of earthworm in As uptake from original As-polluted soil by maize (Zea mays L.), and their effects on As, P fractions in the rhizosphere. The As-polluted soils with three As levels were collected from the arable soil near As mine. The plants were harvested after 10 weeks of growth. Dry weight (DW) and P, As concentrations of plants, as well as As and P fractions of the rhizospheric soil, were determined. The results showed that inoculated earthworm or appended rice straw increased maximal 149%, 222% DW of root and shoot, respectively. At the medium and high soil As levels, root As concentration in the soil treated by earthworm and rice straw was highest among all treatments, and earthworm increased more As concentration of shoot than rice straw did. In different soil As levels, root P concentration in the soil treated by earthworm was highest, and shoot P by rice straw. Ca-P affected maize absorbing As at the low soil As level(r = 0.981), and maize absorbing Al-P was restrained by As involved in well-crystallized hydrous oxides of Fe and Al at the medium (r = 0.953)and high (r = 0.997)soil As levels. The concentration of non-specially absorbed As and As combined with Fe or Al and of O-P increased at the soil inoculated earthworm or/and appended rice straw at the same time. These results indicated that earthworm was more valuable for plant developing than rice straw was.

DNA damage, apoptosis and C-myc, C-fos, and C-jun overexpression induced by selenium in rat hepatocytes.

OBJECTIVE: To study the effects of selenium on DNA damage, apoptosis and c-myc, c-fos, and c-jun expression in rat hepatocytes. METHODS: Sodium selenite at the doses of 5, 10, and 20 micromol/kg was given to rats by i.p. and there were 5 male SD rats in each group. Hepatocellular DNA damage was detected by single cell gel electrophoresis (or comet assay). Hepatocellular apoptosis was determined by TUNEL (TdT-mediated dUTP nick end labelling) and flow cytometry. C-myc, c-fos, and c-jun expression in rat hepatocytes were assayed by Northern dot hybridization. C-myc, c-fos, and c-jun protein were detected by immunohistochemical method. RESULTS: At the doses of 5, 10, and 20 micromol/kg, DNA damage was induced by sodium selenite in rat hepatocytes and the rates of comet cells were 34.40%, 74.80%, and 91.40% respectively. Results also showed an obvious dose-response relationship between the rates of comet cells and the doses of sodium selenite (r=0.9501, P<0.01). Sodium selenite at the doses of 5, 10, and 20 micromol/kg caused c-myc, c-fos, and c-jun overexpression obviously. The positive brown-yellow signal for proteins of c-myc, c-fos, and c-jun was mainly located in the cytoplasm of hepatocytes with immunohistochemical method. TUNEL-positive cells were detected in selenium-treated rat livers. Apoptotic rates (%) of selenium-treated liver cells at the doses of 5, 10, and 20 micromol/kg were (3.72 +/- 1.76), (5.82 +/- 1.42), and (11.76 +/- 1.87) respectively, being much higher than those in the control. Besides an obvious dose-response relationship between apoptotic rates and the doses of sodium selenite (r=0.9897, P<0.01), these results displayed a close relationship between DNA damage rates and apoptotic rates, and the relative coefficient was 0.9021, P<0.01. CONCLUSION: Selenium at 5-20 micromol/kg can induce DNA damage, apoptosis, and overexpression of c-myc, c-fos, and c-jun in rat hepatocytes.

[Effects of selenium on expression of TERT, c-Myc and p53 induced by cadmium in rat liver].

OBJECTIVE: To study the effects of sodium selenite on expression of telomerase reverse transcriptase mRNA, c-Myc and p53 induced by cadmium chloride in rat liver. METHODS: Male SD rats were divided randomly into 6 groups, each group had 5 animals. The groups comprised the control group, Se group (5 micromol/kg sodium selenite), 5 micromol/kg cadmium chloride group, 10 micromol/kg cadmium chloride group, Se (5 micromol/kg sodium selenite) + 5 micromol/kg cadmium chloride group, Se (5 micromol/kg sodium selenite) + 10 micromol/kg cadmium chloride group. After 48 hours of the first injection, the expression of TERT mRNA was measured with RT-PCR and c-Myc, and p53 proteins were measured by immunohistochemistry method. RESULTS: Compared with control group, the expression of TERT was increased in 5 micromol/kg Cd group and 10 micromol/kg Cd group, c-Myc protein was increased in 10 micromol/kg Cd group, and the expression of p53 protein was increased in 5 micromol/kg group and 10 micromol/kg Cd group. TERT expression in Se + 10 micromol/kg Cd group was lower than that of 10 micromol/kg Cd group significantly. c-Myc protein was decreased in Se + 10 micromol/kg Cd group compared with 10 micromol/kg Cd group. p53 protein of Se + 5 micromol/kg Cd group and Se + 10 micromol/kg Cd group were decreased significantly compared with 5 micromol/kg Cd group and 10 micromol/kg Cd group respectively. CONCLUSION: The cadmium at the doses of between 5 and 10 micromol/kg can activate TERT and up-regulate c-Myc and p53 proteins. The selenium at the dose of 5 micromol/kg has the antagonistic effect on expression of TERT, c-Myc and p53 induced by cadmium in rat liver.

Effects of selenium and zinc on renal oxidative stress and apoptosis induced by fluoride in rats.

OBJECTIVE: To study the effects of selenium and zinc on oxidative stress, apoptosis, and cell cycle changes in rat renal cells induced by fluoride. METHODS: Wistar rats were given distilled water containing sodium fluoride (50 mg/L NaF) and were gavaged with different doses of selenium-zinc preparation for six months. Four groups were used and each group had eight animals (four males and four females). Group one, sham-handled control; group two, 50 mg/L NaF; group three, 50 mg/L NaF with a low dose of selenium-zinc preparation (0.1 mg/kg Na2 SeO3 and 14.8 mg/kg ZnSO4 x 7H2O); and group four, 50 mg/L NaF with a high dose of selenium-zinc preparation (0.2 mg/kg Na2 SeO3 and 29.6 mg/kg ZnSO4 x 7H2O). The activities of serum glutathione peroxidase (GSH-Px), kidney superoxide dismutase (SOD), and the levels of malondialdehyde (MDA) and glutathione (GSH) in the kidney were measured to assess the oxidative stress. Kidney cell apoptosis and cell cycle were detected by flow cytometry. RESULTS: NaF at the dose of 50 mg/L increased excretion of fluoride in urine, promoted activity of urine gamma-glutamyl transpeptidase (gamma-GT), inhibited activity of serum GSH-PX and kidney SOD, reduce kidney GSH content, and increased kidney MDA. NaF at the dose of 50 mg/L also induced rat renal apoptosis, reduced the cell number of G2/M phase in cell cycle, and decreased DNA relative content significantly. Selenium and zinc inhibited effects of NaF on oxidative stress and apoptosis, promoted the cell number of G2/M phase in cell cycle, but failed to increase relative DNA content significantly. CONCLUSION: Sodium fluoride administered at the dose of 50 mg/L for six months induced oxidative stress and apoptosis, and changes the cell cycle in rat renal cells. Selenium and zinc antagonize oxidative stress, apoptosis, and cell cycle changes induced by excess fluoride.

[Effects of selenium on rat hepatocellular DNA damage induced by cadmium in vitro].

OBJECTIVES: This study was conducted to explore effects of selenium on rat hepatocellular DNA damage induced by cadmium in vitro. METHOD: Sodium selenite was added at concentrations of 8.75, 17.50 and 35.00 micromol/L respectively with cadmium chloride at the concentrations of 8.75, 17.50 and 35.00 micromol/L respectively and rat hepatocellular DNA damage was measured with single cell gel electrophoresis (comet assay). RESULTS: Sodium selenite at the concentration of 8.75 micromol/L inhibited DNA damage caused by cadmium chloride at the concentration of 8.75, 17.50 and 35.00 micromol/L in rat liver cells (P < 0.05). Although sodium selenite at 17.50 micromol/L inhibited DNA damage induced by cadmium chloride at 17.50 and 35.00 micromol/L, it did not inhibit DNA damage induced by cadmium chloride at 8.75 micromol/L. Sodium selenite at 35.00 micromol/L did not have antagonistic effects on DNA damage induced by cadmium chloride at 8.75, 17.50 and 35.00 micromol/L. In addition, sodium selenite at 8.75 micromol/L had the best antagonistic effect while cadmium chloride at 8.75 micromol/L, but the antagonistic effect of sodium selenite at 17.50 micromol/L was better than 8.75 micromol/L while cadmium chloride at 17.50 and 35.00 micromol/L. CONCLUSION: The antagonistic effect of selenium on rat hepatocellular DNA damage induced by cadmium related to the concentrations of selenium and also to the concentration ratio between selenium and cadmium.

[Effects of selenium on benzo[a] pyrene-induce DNA damage in mouse lung cells].

OBJECTIVE: To explore the effects of selenium on DNA damage induced by benzo[a] pyrene (BaP) in mouse lung cells. METHODS: Sodium selenite was given to Kunming male mice by i.p. and BaP was given by oral gavage. The control group was given solvent only with the same method. DNA damage was detected by single cell gel electrophoresis (or comet assay). RESULTS: The damage degrees in mice treated with 125, 250 and 500 mg/kg of BaP were more severe than that of control (P < 0.01). The rates of comet cells in the BaP-treated groups (43.50%, 84.00%, 95.63%) were significantly higher than that of control (9.75%, P < 0.01), and there was obvious dose-response relationship. 0.75, 1.50 and 3.00 mg/kg of sodium selenite presented antagonistic effects against DNA damage induced by 250 mg/kg of BaP in mouse's lung cells. The antagonistic effect of sodium selenite at the dose of 1.50 mg/kg was better than those of sodium selenite at the doses of 0.75, 3.00 mg/kg. CONCLUSION: BaP at the doses of 125 approximately 500 mg/kg could significantly induce DNA damage of lung cells in mice. 0.75 approximately 3.00 mg/kg of sodium selenite could inhibit DNA damage of lung cells in mice induced by 250 mg/kg of BaP.