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Tong Shen

Publications and source records attributed to Tong Shen.

8 recordsLinked to original sources

Lipidomic Profiling Reveals Differential Behaviors of Individual Free Fatty Acids During Altered Metabolic States in Rats.

We used lipidomic analyses to investigate how individual free fatty acids (FFAs) behave differently in metabolic states altered by diet and by antibiotic treatment (ABX) that depletes gut bacteria. Wistar rats were fed either a low-fat or high-fat purified diet, or standard chow with or without antibiotics for two weeks (n = 8-10). Blood samples were then collected before and after meals. Individual FFAs were quantified and grouped based on distinct postprandial response patterns across dietary and treatment conditions. Eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), key ω-3 FFAs, exhibited postprandial shifts suggestive of suppressed adipocyte lipolysis following meals. Fatty acids in the high-fat diet (HFD) elevated postprandial FFA levels, masking the meal-induced suppression of lipolysis observed with chow or low-fat diet (LFD). Some FFAs, including medium-chain saturated species, remained unaffected by meals. We further evaluated the impact of diet and ABX on baseline (pre-meal) concentrations of FFAs. Certain FFAs were altered by purified diets compared to standard chow. Notably, EPA and DHA were selectively depleted under HFD conditions, likely due to enhanced catabolic activity. In conclusion, lipidomic profiling revealed divergent behaviors among individual FFAs, reflecting distinct metabolic processes and regulatory mechanisms under altered metabolic states.

Animals↗

Two new benzofurans and other constituents from Ligularia przewalskii.

Two new benzofurans, 2-(1,2-dihydroxyisopropyl)-5,6-dimethoxybenzofuran (1) and 2-(1-O-feruloyl-2-hydroxyisopropyl)-5,6-dimethoxybenzofuran (2), along with eleven known compounds (3-13) were isolated from the roots of Ligularia przewalskii. Their structures were established on the basis of spectroscopic methods. The antibacterial activity of compounds 1 and 3-5 was tested.

Anti-Bacterial Agents↗

[Effects of TCE and PCE on cultured human keratinocyte lipid peroxidation and protective effect of vitamin E on it].

OBJECTIVE: To explore the different concentrations of trichloroethylene (TCE) or perchloroethylene (PCE) induced cultured normal human epidermal keratinocyte (KC) lipid peroxidation and protective effect of Vitamin E on it. METHODS: KC derived from 3 or more donors were pooled together and cultured with K-SFM. Neutral Red Uptake Assay was used to determine the IC50 of TCE or PCE, and then different concentrations of TCE or PCE were administered for culturing KC; 0.5 mmol/L TCE or 0.2 mmol/L PCE and different concentrations of Vitamin E were used to determine the protective effect of Vitamin E. After 4 hours' culture, kits were used to determine cellular MDA, SOD and ROS level. RESULTS: Treatment of KC with different concentrations of TCE or PCE showed significant dose-related variations in lipid peroxidation, with the higher concentration, higher level of MDA, ROS and lower activity of SOD displayed in this study. Vitamin E 10 - 200 mmol/L dose-dependently attenuated MDA and ROS level, and increased SOD activities. CONCLUSION: TCE or PCE can induce the lipid peroxidation in cultured KC and Vitamin E protects it from TCE- or PCE-induced peroxidation.

Antioxidants↗

Cytotoxicity of trichloroethylene and perchloroethylene on normal human epidermal keratinocytes and protective role of vitamin E.

Trichloroethylene (TCE) and perchloroethylene (PERC), the most common alkenyl halides, have been extensively used in industry, and can cause skin damage. To evaluate their cytotoxic potential on skin, the effects of these agents on the normal human epidermal keratinocytes (NHEK) were investigated. Their action on cell viability, membrane integrity and lipid peroxidation (LPO) was assessed by neutral red uptake (NRU) assay, lactate dehydrogenase (LDH) release test and measurement of malondialdehyde (MDA) levels and superoxide dismutase (SOD) activity. In addition, the protective effect of antioxidatant vitamin E on the cytotoxicity was also studied. Incubation of NHEK with various concentrations (0.01-31.6 mM) of TCE or PERC caused a dose-dependent decrease in cell viability, with 80% reduction at 31.6 mM. NR50 values from the cytotoxicity assay was found to be 4.53 and 2.16 mM for TCE and PERC, respectively. A time- and concentration- dependent release of LDH were observed at 1, 2, 3, 4 h after cells were exposed to different doses of TCE or PERC. These agents also caused an increase of MDA, whilst an inhibition of SOD activity, in a concentration-dependent manner. Pre-treatment of the cells with vitamin E at 10-200 mM dose-dependently attenuated the cytotoxic effect of TCE or PERC. Pre-treatment with vitamin E also reversed subsequent TCE or PERC-induced release of LDH, elevation of lipid peroxidation and decline of anti-oxidant enzyme activities. These results suggest that TCE and PERC could induce cytotoxicity to NHEK associated with oxidative stress and antioxidatant vitamin E could effectively protect NHEK from TCE- or PERC-induced cytotoxicity, which may be associated to the superoxide scavenging effect and enhancement of anti-oxidant enzyme activities.

Cell Survival↗

[Relationship of nitric oxide with the apoptosis of keratinocytes].

Nitric oxide (NO) is a kind of free radical, also is a signaling molecule, which universally distributed in the tissues of organism. NO play important role in the dermato-, cardia-, encephalo-, hepat- and immunological regulation on the physio- and patho- situation. Recently studying show that NO can bifunctionally regulate the apoptosis of keratinocytes, which play an important role in the occurrence and development of many skin diseases. However, the regulatory mechanism still can't be completely elucidated at present time. In this review, we are reviewing the recent investigation progress on the apoptosis of keratinocytes and some diseases of skin that related to the regulating disturbance of NO.

Apoptosis↗

[Study of trichloroethylene-induced apoptosis in normal human epidermis keratinocytes in vitro].

OBJECTIVE: To investigate the apoptosis-inducing effect of trichloroethylene (TCE) on cultured normal human epidermis keratinocytes (NHEK) in vitro. METHODS: NR(50) values (the concentration of neutral red absorbed is reduced to 50%) of TCE on NHEK were assayed by neutral red uptake (NRU), and the administered dose of TCE was determined. Lipid peroxidation (LPO) and oxidative stress were assessed by measurement of malondialdehyde (MDA) contens and superoxide dismutase (SOD) activity. Transmission electron microscope (TEM) were used to observe morphologic changes, flow cytometer (FCM) was used to measure DNA contents and calculate cell apoptosis rate and proliferation index (PI). RESULTS: NR(50) values of TCE on NHEK was found to be 4.53 mmol/L (95% CI: 3.92-5.13 mmol/L). The increase in MDA content and inhibition of SOD activity in a concentration-dependent manner were shown after NHEK was treated with a series of dose of TCE 4 h later, and typical morphologic changes of apoptosis were also observed by TEM examination. FCM analysis revealed a sub-G(1) peak in the apoptotic cells. The apoptotic rate in TCE 0.125, 0.500, 2.000 mmol/L exposed groups (31.83%, 38.63%, 44.35%, respectively) were significantly higher than that in blank control (18.42%), while PI in TCE 0.125, 0.500, 2.000 mmol/L group (3.26%, 2.48%, 2.07%, respectively) were significantly lower than that in blank control (4.99%). CONCLUSION: TCE may induce apoptosis of cultured NHEK in vitro, and inhibit cell proliferation through lipid peroxidation and oxidative stress.

Apoptosis↗