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Polysaccharide of Balanophora involucrata Hook. f. (BPS), the major component of Balanophora involucrata Hook. f., was confirmed the protective effect on liver injury in our previous study. This research aimed to investigate the protective mechanism of BPS on experimental liver injury by attenuating cell ferroptosis through modulating solute carrier family 7 member 11/glutathione peroxidase 4 (SLC7A11/GPX4) pathway. The animal experiment was approved by the Experimental Animal Ethical Committee of Hubei Minzu University and all rats had received human care in compliance with the institutional animal care guidelines. Rats were given intraperitoneal injection of (D-galactosamine, D-GalN) solution (800 mg·kg-1) one time to establish the acute liver injury model. The results showed aspartate amino transferase (AST), alanine aminotransferase (ALT) and 4-hydroxynonenal (4-HNE) levels in serum were decreased, and the contents of reactive oxygen species (ROS), Fe2+, malondialdehyde (MDA) and lipid peroxide (LPO) in liver tissues also decreased and glutathione (GSH) level increased after BPS administration with 200 mg·kg-1. Besides, BPS reduced iron deposition and increased the expression of SLC7A11 and GPX4 proteins in liver tissue. In conclusion, BPS ameliorated experimental liver injury by alleviating cell ferroptosis through SLC7A11/GPX4 pathway. The present study pointed to the possibility of utilizing BPS for protection against liver injury in clinic.
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Aim To study the therapeutic effect of Balanophora polysaccharide(BPS)on gastric ulcer(GU)induced by acetic acid in rats and to investigateits mechanisms. Methods Sixty male SD rats were randomly divided into sham-operated group, GU model group, omeprazole positive group(3.6 mg·kg-1), and low, medium and high dose of BPS treatment groups(100, 200 and 400 mg·kg-1). The GU model group was prepared by acetic acid cautery method, and the morphology and pathological changes of ulcers were observed by visual observation combined with HE staining, and the ulcer area and inhibition rate were measured and calculated; superoxide dismutase(SOD)activity, malondialdehyde(MDA)content and glutathione peroxidase(GSH-PX)activity were measured by enzymatic assay; tumor necrosis factor-α(TNF-α)and interleukin-6(IL-6)content were detected by ELISA. The expression levels of epidermal growth factor(EGF)and epidermal growth factor receptor(EGFR)were measured by immunohistochemistry staining and Western blot. Results Compared with the sham-operated group, obvious ulcer damage was seen in the model group. Compared with the model group, the BPS-treated group showed a significant reduction in ulcer area, an increase in SOD and GSH-PX activity and EGF and EGFR expression levels, and a significant decrease in MDA, TNF-α and IL-6 content. Conclusions BPS has a therapeutic effect on GU in rats, and its mechanism may be related to the inhibition of oxidative stress, suppression of inflammatory stimuli and promotion of regenerative repair of gastric mucosa.
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This study was designed to investigate the effect of dihydromyricetin (DHM) on inducing apoptosis of ovarian cancer cells A2780 through endoplasmic reticulum stress (ERS) pathway and the mechanisms involved in vitro and in vivo. A2780 cells were treated with different concentrations of DHM, and the protein expression levels of glucose-regulated protein 78 (GRP78) which is related to ERS increased, apoptotic proteins C/EBP-homologous protein (CHOP), and cysteinyl aspartate specific proteinase-12 (caspase-12) elevated. After pretreatment with ERS inhibitor, 4-phenyl butyric acid (4-PBA), following the intervention with DHM, the A2780 cell viability decreased and apoptotic rate increased. All animal welfare and experimental procedures were approved by the Animal Ethics Committee of Chongqing Medical University. Intraperitoneal injection of DHM suspension into nude mice with ovarian cancer could significantly inhibit the growth of transplanted tumor in vivo, increase the protein expression levels of GRP78, CHOP, and caspase-3. Moreover, swollen and broken endoplasmic reticulum could be observed in tumor tissues, suggesting that DHM intervention induces apoptosis mediated by ERS. The results indicated that DHM could induce apoptosis of ovarian cancer cells and inhibit the growth of transplanted tumors in nude mice, which might be related to the activation of ERS pathway.
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Objective:To explore the effect of trillin on oxidative stress response and nuclear factor E2-related factor 2/antioxidant response element (Nrf2/ARE) pathway in rats after spinal cord injury (SCI). Methods:A total of 108 male Sprague-Dawley rats were randomly divided into sham group (n = 36), model group (n = 36) and trillin group (n = 36), each group was divided into one day, three days and seven days subgroups, with twelve rats in each subgroup. The SCI model was established by modified Allen's heavy strike method in the model group and the trillin group, but no obvious injury in the sham group. The trillin group was given trillin 200 mg/kg every day, and the same amount of normal saline was given in the sham group and model group, twice a day. BBB score was performed one day, three days and seven days after modeling. Morphological changes were tested by Nissl's staining, and the changes of malonaldehyde (MDA) content and superoxide dismutase (SOD) activity were detected by ELISA seven days after modeling. The expression of Nrf2, Kelch like ECH associated protein 1 (Keap1), NAD(P)H quinone oxidoreductase (NQO1) and haemoxygenase 1 (HO-1) were detected by Western blotting one day, three days and seven days after modeling. Results:Compared with the model group, BBB scores increased (P < 0.05); the structure of spinal cord was more complete and the number of Nissl bodies increased; SOD activity increased (P < 0.05) and MDA content decreased (P < 0.05); the expression of Nrf2, Keap1, NQO1 and HO-1 increased (P < 0.05) in the trillin group. Conclusion:Trillin may play a protective role in spinal cord injury by inhibiting oxidative stress response and improving the motor function.
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Objective:To delineate the distribution and abundance of interleukin 17 receptor mRNA in normal tissues of rhesus macaques.Methods:Tissue samples were collected from different systems including lymphoid system,digestive system and genital system and the mRNA levels of IL-17RA and IL-17RC were examined by real time RT-PCR.Meanwhile the levels of IL-17RA and IL-17RC mRNA in the PBMCs of rhesus macaques,African green monkeys and cynomolgus monkeys were examined.Results:IL-17RA mRNA was expressed in all the tested tissues and the levels were significantly different among these systems (P＜0.05).IL-17RC mRNA level in the large intestine was higher than that in the small intestine.IL-17RA mRNA level in rhesus macaque PBMCs was 3 and 5 times higher than that of cynomolgus monkeys and African green monkeys respectively,while IL-17RC mRNA in the PBMCs was below the limit of detection.Conclusion:IL-17RA is widely distributed in rhesus macaques;the expression level is different among different tissues and species.
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<p><b>OBJECTIVE</b>To explore the effect of Se-riched soybean peptide (SSP) on antioxidant function in rats of fatty liver caused by high-fat diet.</p><p><b>METHODS</b>Forty Wistar rats were divided into 4 groups randomly and fed with standard diet and water (NC), high-fat diet and water (HC), high-fat diet and SSP (0.1 g/d) (SeH), standard diet and SSP (0.1 g/d) (SeN) respectively. After 10 weeks, the rats were killed to investigate the pimelosis level in liver tissues by Sudan III staining and the expression of hepatic GRP78 by immunohistochemical analysis. We also analyzed the changes of liver function, blood lipid, the glutathione peroxidase (GSH-Px), superoxide dismutase (SOD) activity and malondialdehyde (MDA) content in livers and serum.</p><p><b>RESULTS</b>The pimelosis level, total cholesterol (TC), triglyceride (TG), MDA contents and the expression of GRP78 in HC group were significantly higher than those in NC, SeN, SeH groups. The activities of GSH-Px and SOD in liver and serum were markedly up-regulated in SeH (P < 0.01). There was no significant difference between NC and SeN groups.</p><p><b>CONCLUSION</b>SSP can improve liver cell injury and the antioxidant functions in rats with fatty liver effectively and decrease the expression of GRP78 in liver.</p>
Subject(s)
Animals , Male , Rats , Antioxidants , Metabolism , Diet, High-Fat , Disease Models, Animal , Fatty Liver , Metabolism , Heat-Shock Proteins , Metabolism , Liver , Metabolism , Rats, Wistar , Selenium , Pharmacology , Soybean Proteins , Pharmacology , Glycine max , ChemistryABSTRACT
<p><b>OBJECTIVE</b>To study the urinary excretion pattern for of 2-thio-thiazolidine-4-carboxylic acid (TTCA) in workers exposed to CS2, so as to provide experimental basis for working out biomonitoring measures for short-term exposure to CS2.</p><p><b>METHODS</b>Sixty-nine subjects were divided into three groups: (1) fourteen volunteers who had not been exposed to CS2 before were exposed to CS2 for 2 hours, their urine samples were collected and analyzed at different time points; (2) The urine samples of 15 occupational exposure workers were collected on pre-shift, mid-shift, post-shift; (3) The relationship between 8 h time weighted average CS2 exposure concentrations (PC-TWA) and TTCA levels of post-shift urine was studied among 40 workers chronically exposed to CS2.</p><p><b>RESULTS</b>(1) In the 1st group, urine TTCA level reached the peak [(1.03 +/- 0.72) mg/gCr] 4 h after exposure; (2) In the 2nd group, urine TTCA level on pre-shift [(0.37 +/- 0.28) mg/gCr] was lower than that on mid-shift [(1.23 +/- 0.71) mg/gCr, P<0.01] and post-shift [(1.31 +/- 0.78) mg/gCr, P<0.01]; (3) In the 3rd group, there was a linear relationship between the post-shift urine TTCA level and 8 h CS2 exposure concentrations dose (PC-TWA). The regression equation is Y(TTCA mg/gCr)=1.163 6X(CS2 mg/m3)-5.411 6.</p><p><b>CONCLUSION</b>The post-shift urine TTCA levels may be regarded as a bio-monitoring index for workers exposed to CS2.</p>