Interference of altered plasma trace elements profile with hyperhomocysteinemia and oxidative stress damage to insulin secretion dysfunction in Psammomys obesus: focus on the selenium

At present, there are few reports concerning the relationship between miR-122 and diabetes. In addition, the effect of miR-122 on streptozotocin- (STZ-) induced oxidative damage in INS-1 cells remains unclear. The present study aimed to investigate the role and modulatory mechanisms involving miR-122 in diabetes. STZ was used to induce INS-1 cell damage. Reverse transcription-quantitative PCR was used to investigate the expression of miR-122. A TUNEL cell apoptosis detection kit was used to detect apoptosis. Intracellular ROS levels were determined using dichlorofluorescein-diacetate. The activities of insulin secretion, superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-px) were measured using ELISA kits. Western blotting was used to measure the expression levels of Bax, Bcl-2, PI3K, p-PI3K, caspase-3 and caspase-9, cleaved-caspase-3 and cleaved-caspase-9, AKT, and p-AKT. Then, LY294002 (LY, PI3K inhibitor) was used to treat INS-1 cells, and oxidative stress and apoptosis were measured. The results showed that STZ-induced inhibitory effects on insulin secretion were mitigated by miR-122 inhibitor, and the activities of SOD, CAT, and GSH-px were also increased. Furthermore, miR-122 inhibitor inhibited apoptosis and oxidative stress in STZ-induced INS-1 cells. Finally, the addition of LY increased insulin levels; reduced the activities of SOD, CAT, and GSH-px; and promoted apoptosis in STZ-induced INS-1 cells. In conclusion, interference with miR-122 can inhibit oxidative stress and apoptosis in STZ-induced INS-1 cells, involving a mechanism of action related to the PI3K/AKT pathway.

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Mangifera indicaFruit Extract Improves Memory Impairment, Cholinergic Dysfunction, and Oxidative Stress Damage in Animal Model of Mild Cognitive Impairment

Oxidative Medicine and Cellular Longevity ◽

10.1155/2014/132097 ◽

2014 ◽

Vol 2014 ◽

pp. 1-7 ◽

Cited By ~ 11

Author(s):

Jintanaporn Wattanathorn ◽

Supaporn Muchimapura ◽

Wipawee Thukham-Mee ◽

Kornkanok Ingkaninan ◽

Sakchai Wittaya-Areekul

Keyword(s):

Oxidative Stress ◽

Animal Model ◽

Cognitive Impairment ◽

Mild Cognitive Impairment ◽

Memory Impairment ◽

Cholinergic Neurons ◽

Protective Agent ◽

Cholinergic Dysfunction ◽

Stress Damage ◽

And Oxidative Stress

To date, the effective preventive paradigm against mild cognitive impairment (MCI) is required. Therefore, we aimed to determine whetherMangifera indicafruit extract, a substance possessing antioxidant and cognitive enhancing effects, could improve memory impairment, cholinergic dysfunction, and oxidative stress damage in animal model of mild cognitive impairment. Male Wistar rats, weighing 180–200 g, were orally given the extract at doses of 12.5, 50, and 200 mg·kg−1BW for 2 weeks before and 1 week after the bilateral injection of AF64A (icv). At the end of study, spatial memory, cholinergic neurons density, MDA level, and the activities of SOD, CAT, and GSH-Px enzymes in hippocampus were determined. The results showed that all doses of extract could improve memory together with the decreased MDA level and the increased SOD and GSH-Px enzymes activities. The increased cholinergic neurons density in CA1 and CA3 of hippocampus was also observed in rats treated with the extract at doses of 50 and 200 mg·kg−1BW. Therefore, our results suggested thatM. indica, the potential protective agent against MCI, increased cholinergic function and the decreased oxidative stress which in turn enhanced memory. However, further researches are essential to elucidate the possible active ingredients and detail mechanism.

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Linkage of Some Trace Elements, Peripheral Blood Lymphocytes, Inflammation, and Oxidative Stress in Patients Undergoing Either Hemodialysis or Peritoneal Dialysis

Peritoneal Dialysis International ◽

10.3747/pdi.2009.00225 ◽

2011 ◽

Vol 31 (5) ◽

pp. 583-591 ◽

Cited By ~ 30

Author(s):

Chih-Hung Guo ◽

Chia-Liang Wang ◽

Pei-Chung Chen ◽

Te-Cheng Yang

Keyword(s):

Oxidative Stress ◽

Trace Elements ◽

Peritoneal Dialysis ◽

T Lymphocytes ◽

Trace Element ◽

T Lymphocyte ◽

Immune Status ◽

Dialysis Patients ◽

Markers Of Oxidative Stress ◽

And Oxidative Stress

BackgroundChanges in essential trace elements may affect the inflammatory and immunological state of patients on hemodialysis (HD) or peritoneal dialysis (PD). Therefore, we aimed to determine trace element content and markers of oxidative stress, inflammation, and immune status in HD and PD patients and to assess the relationships among these parameters.MethodsPatients on either HD ( n = 20) or PD ( n = 20) and age-, sex-, body mass index-matched healthy individuals ( n = 20) were enrolled in the study. The trace elements zinc, copper, selenium, and iron; markers of oxidative stress thiobarbituric acid reactive substances (TBARS) and protein carbonyl levels; activities of antioxidant enzymes superoxide dismutase (SOD), glutathione peroxidase (GPx), and catalase; percentages of CD3 T lymphocytes and the subsets CD4 and CD8; the CD4/CD8 ratio; and C-reactive protein (CRP) were measured.ResultsAll dialysis patients had low levels of albumin and hemoglobin. Significantly decreased percentages of CD3 and CD4 T lymphocytes and increased levels of CRP, TBARS, and carbonyl compounds were observed in HD patients. HD patients also had elevated erythrocyte SOD, lower GPx and catalase activities, and decreased levels of Se, Zn, and Fe in comparison to PD patients and healthy subjects. In addition, CRP was positively associated with TBARS and carbonyl levels, but was significantly inversely associated with Zn and Se levels. Positive correlations were found between T lymphocyte CD3 and CD4 percentages and Zn, Se, and Fe levels.ConclusionsThere were significant decreases in T lymphocyte-related immunological regulation and increased inflammation and oxidative stress in dialysis patients. Essential trace element status was independently related to immune status, inflammation, and oxidative damage.

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