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Ascorbate (AsA) is the most abundant antioxidant in plant cells and a cofactor for a large number of key enzymes. However, the mechanism of how AsA levels are regulated in plant cells remains unknown. The Arabidopsis (Arabidopsis thaliana) activation-tagged mutant AT23040 showed a pleiotropic phenotype, including ozone resistance, rapid growth, and leaves containing higher AsA than wild-type plants. The phenotype was caused by activation of a purple acid phosphatase (PAP) gene, At PAP15, which contains a dinuclear metal center in the active site. AtPAP15 was universally expressed in all tested organs in wild-type plants. Overexpression of AtPAP15 with the 35S cauliflower mosaic virus promoter produced mutants with up to 2-fold increased foliar AsA, 20% to 30% decrease in foliar phytate, enhanced salt tolerance, and decreased abscisic acid sensitivity. Two independent SALK T-DNA insertion mutants in AtPAP15 had 30% less foliar AsA and 15% to 20% more phytate than wild-type plants and decreased tolerance to abiotic stresses. Enzyme activity of partially purified AtPAP15 from plant crude extract and recombinant AtPAP15 expressed in bacteria and yeast was highest when phytate was used as substrate, indicating that AtPAP15 is a phytase. Recombinant AtPAP15 also showed enzyme activity on the substrate myoinositol-1-phosphate, indicating that the AtPAP15 is a phytase that hydrolyzes myoinositol hexakisphosphate to yield myoinositol and free phosphate. Myoinositol is a known precursor for AsA biosynthesis in plants. Thus, AtPAP15 may modulate AsA levels by controlling the input of myoinositol into this branch of AsA biosynthesis in Arabidopsis. [ABSTRACT FROM AUTHOR]

[Objectives] This study was conducted to investigate the renal protective effects of Wuling Powder on mice with nephrotic syndrome (NS) based on Notch pathway. [ Methods ] Sixty KM mice were randomly divided into normal group, model group, prednisone acetate positive group, high-dose Wuling Powder group, medium-dose Wuling Power group and low-dose Wuling Power group, with 10 mice in each group. Three days after prophylactic administration, a comprehensive nephropathy model was prepared by injecting 1 mg/ml doxorubicin hydrochloride solution (7.5 mg/kg) into the tail vein. After successful modeling, prednisone acetate and Wuling SAN were given high, medium and low doses for intervention for 28 d, respectively. After that, urinary protein and creatinine contents of mice in each group were detected, and pathological damage of renal tissue was observed by HE and Masson staining. The mRNA levels of Notchl, Jaggedl and Hesl in mouse kidney tissues were detected by RT-PCR, and the expression levels of Notchl, Jaggedl and Hesl proteins were detected by Western blot. [Results] Wuling Powder could effectively reduce the contents of urine protein (P <0. 01) and Scr (P <0. 01) in NS mice, and alleviate the pathological injury of kidney. Compared with the model group, the prednisone acetate group and various Wuling Powder groups could down-regulate the expressions of Notchl, Jaggedl and Hesl mRNA in the kidney tissue of mice (P<0. 01), and the expression of Notchl protein in the renal tissue of mice decreased (P<0.01). The contents of Hesl in the prednisone acetate group and the high- and medium-dose Wuling Powder groups significantly decreased (P <0. 05). [ Conclusions] Wuling Powder could protect the kidneys in mice with NS through Notch pathway. [ABSTRACT FROM AUTHOR]

There is strong evidence that β-amyloid (Aβ) causes oxidative stress and induces mitochondrial dysfunction in the pathogenesis of Alzheimer’s disease. Mitochondrial transcription factor A (Tfam) has multiple roles in the maintenance of mtDNA. To study the protective roles of Tfam against amyloid neurotoxicity, we established SH-SY5Y cell lines stably overexpressing Tfam and exposed them to 10 μm Aβ1-42 for 24 h. We found that Tfam overexpression attenuated Aβ1-42-induced cell viability damage and apoptosis. In addition, Tfam overexpression significantly suppressed the increase in excess reactive oxygen species and reversed the reduction in cytochrome c oxidase activity and ATP production induced by Aβ1-42. Furthermore, overexpression of ΔC-Tfam, which has no functional domain for stimulating mtDNA transcription but can still maintain the mtDNA nucleoid formation and mtDNA copy number, also exhibited protective effects against Aβ1-42 cytotoxicity in SH-SY5Y cells. Together, our data suggest that Tfam overexpression protects mitochondria against Aβ-induced oxidative damage in SH-SY5Y cells. These beneficial effects may be attributable to the roles of Tfam in maintaining mtDNA nucleoid formation and mtDNA copy number. [ABSTRACT FROM AUTHOR]