Diagnostic Significance of Serum Levels of Nerve Growth Factor and Brain Derived Neurotrophic Factor in Diabetic Peripheral Neuropathy.

BACKGROUND Our study aimed to explore the levels of nerve growth factor (NGF) and brain derived neurotrophic factor (BDNF) in healthy participants, type 2 diabetes mellitus (T2DM) patients, and diabetic peripheral neuropathy (DPN) patients in order to find their effects on DPN. MATERIAL AND METHODS The clinical data of 110 healthy participants (age: 57.3±8.2 year, height: 165.4±5.5 cm, weight: 64.1±7.5 kg), 83 T2DM patients (age: 56.5±7.9 year, height: 164.8±6.2 cm, and weight: 63.6±6.6 kg), and 65 DPN patients (age: 58.2±7.3 year, height: 166.7±6.7 cm, weight: 63.1±5.8 kg) were observed. ELISA was applied to detect serum NGF and BDNF levels. Receiver operating characteristic (ROC) curve analysis was performed to evaluate diagnostic value of serum NGF and BDNF levels in DPN. Logistic regression analysis was performed to analyze risk factors for DPN. RESULTS Serum NGF and BDNF levels decreased most in DPN patients. Subsequently, we determined that serum NGF and BDNF levels were correlated with: the course of disease for patients, fasting C-peptide (FCP), 2-hour postprandial C-peptide level (2-h PCP), glycosylated hemoglobin level (HbAlc), and 24-hour urinary microalbumin excretion (24-h UME). ROC curve analysis identified high sensitivity, specificity, and accuracy of NGF and BDNF levels on DPN. Serum levels of NGF and BDNF, course of disease, 2-h PCP level, and postprandial blood glucose level were determined to be risk factors for DPN. CONCLUSIONS Our study highlights that serum levels of NGF and BDNF might be associated with the occurrence and development of DPN.

Role and Mechanism of Keap1/Nrf2 Signaling Pathway in the Regulation of Autophagy in Alleviating Pulmonary Fibrosis.

A variety of internal and external lung diseases may eventually lead to pulmonary fibrosis, and insufficient autophagy is closely related to pulmonary fibrosis. This research is aimed to explore the mechanism of autophagy to alleviate pulmonary fibrosis. Then, a mouse model of pulmonary fibrosis induced by boromycin and histopathological lesions of the lungs of mice were observed by HE staining, which Masson staining assessed the degree of fibrosis in the lung tissue by detecting the expression of hydroxyproline in the tissue. RT-qPCR and western blotting were used to detect the levels of autophagy and Keap1/Nrf2 signaling pathway-related proteins. It was proved that autophagy-related proteins MAP1LC3(LC3) and Beclin 1 were decreased in mice with pulmonary fibrosis, while the expression of p62 was increased. Mice with pulmonary fibrosis worsened after injection of a 3-MA autophagy inhibitor, while injection of autophagy activation of rapamycin agent promoted Nrf2 nuclear mobilization. In a word, autophagy relieves pulmonary fibrosis through the activation of the Keap1/Nrf2 signaling pathway.