Int J Med Sci
-
Diabetes mellitus (DM) is caused by either destruction of pancreatic β-cells (type 1 DM) or unresponsiveness to insulin (type 2 DM). Conventional therapies for diabetes mellitus have been developed but still needs improvement. Many diabetic patients have complemented conventional therapy with alternative methods including oral supplementation of natural products. ⋯ For the type 2 DM model, mice were given high-fat diet for 60 days and then orally administered EGb 761 every other day for 80 days. We found that mice given a high-fat diet and EGb 761 showed decreased blood triglyceride levels, increased liver LPL, increased liver PPAR-α and decreased body weight compared to mice given high-fat diet alone. These results suggest that EGb 761 can exert protective effects in both type 1 and type 2 DM murine models.
-
Antiseptic agents can cause skin irritation and lead to severe problems, especially for individuals with atopic diatheses. We investigated the effect of 4 different antiseptic agents using an atopic dermatitis (AD) model mouse. NC/Nga mice were subcutaneously injected with mite allergen (Dp) to induce AD-like skin lesions (ADSLs), and an application of 0.2% (w/v) benzalkonium chloride (BZK), 10% (w/v) povidone-iodine (PVP-I), 80% (v/v) ethanol (Et-OH), or 0.5% (v/v) chlorhexidine gluconate (CHG) was applied to the ear envelope. ⋯ No differences in any parameters were observed between CHG and the vehicle. Collectively, the results suggest the severity of the ADSL was related in part to the strength of the immunoreaction. These findings suggest that CHG could offer the lowest risk of inducing ADSL in individuals with atopic dermatitis and that medical staff and food handlers with AD could benefit from its use.
-
One of the earliest neuropathological events in Alzheimer's disease is accumulation of astrocytes at sites of Aβ1-42 depositions. Our results indicate that Aβ1-42 toxic peptide increases lipid peroxidation, apoptosis and cell death in neurons but not in astrocytes in primary culture. Aβ1-42-induced deleterious neuronal effects are not present when neurons and astrocytes are mixed cultured. ⋯ In astrocytes Aβ1-42 decreases protein expressions of sirtuin 1 (SIRT-1) and peroxisome proliferator-activated receptor γ (PPAR-γ) and over-expresses peroxisome proliferator-activated receptor γ coactivator 1 (PGC-1) and mitochondrial transcription factor A (TFAM), protecting mitochondria against Aβ1-42-induced damage and promoting mitochondrial biogenesis. In summary our data suggest that astrocytes may have a key role in protecting neurons, increasing neural viability and mitochondrial biogenesis, acquiring better oxidative stress protection and perhaps modulating inflammatory processes against Aβ1-42 toxic peptide. This might be a sign of a complex epigenetic process in Alzheimer's disease development.