Cyanidin-3-O-glucoside attenuates high glucose-induced podocyte dysfunction by inhibiting apoptosis and promoting autophagy via activation of SIRT1/AMPK pathway.

Diabetic nephropathy (DN) is a common and complicated chronic kidney disease around the world. To elucidate and find effective therapies of DN is of vital importance. In this paper, we have discovered that cyanidin-3-O-glucoside (C3G), which is one of the anthocyanins, could alleviate high glucose-induced podocyte dysfunction. MTT, flow cytometry assay, and Western blot analysis showed that C3G could reverse the increase of cell apoptosis under high glucose treatment in MPC5 cells by upregulation of Bcl2 and downregulation of Bax and cleaved caspase-3. Moreover, C3G improved the autophagy decrease that was induced by high glucose through regulating the expression level of LC3-II/LC3-I, Beclin1, and p62. In addition, C3G inhibited epithelial-mesenchymal transition (EMT) by increasing E-cadherin and reducing Vimentin. By further study of the mechanisms, we found C3G activated the SIRT1 and AMPK which were inhibited in high glucose condition. Silencing SIRT1 blocked the effect of C3G on regulating cell apoptosis, autophagy, and EMT. In summary, our current findings suggest the protective effect of C3G against high glucose-induced podocyte dysfunction is by improving autophagy and reducing apoptosis and EMT via activating SIRT1/AMPK pathway. It might be a new insight for the treatment of DN.

The fluorescence of a mercury probe based on osthol.

The ability of osthol (OST) to recognize mercury ions in aqueous solution was studied using fluorescence, UV-vis spectrophotometry, mass spectrometry, and 1H NMR spectroscopy, and the recognition mechanism is discussed. The results showed that OST and Hg2+ can form a complex with a stoichiometric ratio of 1:1. The binding constant was 1.552 × 105 L∙mol-1, having a highly efficient and specific selectivity for Hg2+. The fluorescence intensity of OST showed a good linear correlation with the Hg2+ concentration (6.0 × 10-5 to 24.0 × 10-5 mol∙L-1, R 2 = 0.9954), and the detection limit of the probe was 5.04 × 10-8 mol∙L-1, which can be used for the determination of Hg2+ traces.

Host-guest interaction and properties of cucurbit[8]uril with chloramphenicol.

The interaction between cucurbit[8]uril (Q[8]) and chloramphenicol (CPE) was investigated using single-crystal X-ray diffraction spectroscopy, isothermal titration calorimetry (ITC) and UV-vis, NMR and IR spectroscopy. The effects of Q[8] on the stability, in vitro release performance and antibacterial activity of CPE were also studied. The results showed that CPE and Q[8] formed a 1:1 inclusion complex (CPE@Q[8]) with an inclusion constant of 5.474 × 105 L/mol. The intervention of Q[8] did not affect the stability of CPE, but obviously reduced the release rate of CPE in artificial gastric and intestinal juice; Q[8] has a slow-release effect on CPE. The antibacterial results showed that the minimum inhibitory concentration (MIC) of CPE and CPE@Q[8] toward Escherichia coli (E. coli) was 1.5 × 10-3 and 1.0 × 10-3 mol/L, respectively, and toward Staphylococcus aureus (S. aureus), the MIC was 2.0 × 10-3 mol/L for both CPE and CPE@Q[8]. Therefore, Q[8] enhanced the inhibitory activity of CPE against E. coli.

Host-guest interaction of cucurbit[8]uril with oroxin A and its effect on the properties of oroxin A.

In this study, we investigated the host-guest interactions between oroxin A (OA) and cucurbit[8]uril (Q[8]) using 1H NMR, MS, UV-vis and IR spectroscopy. The results showed that OA and Q[8] formed an inclusion compound (OA@Q[8]) with a molar ratio of 1:1 and a binding constant of 1.299 × 107 L·mol-1. In addition, the effect of Q[8] on the properties of OA was investigated through comparative experiments. The solubility of OA in water increased 22.47-fold when the concentration of Q[8] was 1 × 10-4 mol·L-1. Q[8] hardly affected the antioxidant capacity of OA, while the cumulative release of OA in gastric juice increased 2.3-fold after forming the inclusion compound with Q[8].

Vitamin C mitigates oxidative stress and tumor necrosis factor-alpha in severe community-acquired pneumonia and LPS-induced macrophages.

Oxidative stress is an important part of host innate immune response to foreign pathogens. However, the impact of vitamin C on oxidative stress and inflammation remains unclear in community-acquired pneumonia (CAP). We aimed to determine the effect of vitamin C on oxidative stress and inflammation. CAP patients were enrolled. Reactive oxygen species (ROS), DNA damage, superoxide dismutases (SOD) activity, tumor necrosis factor-alpha (TNF-α), and IL-6 were analyzed in CAP patients and LPS-stimulated macrophages cells. MH-S cells were transfected with RFP-LC3 plasmids. Autophagy was measured in LPS-stimulated macrophages cells. Severe CAP patients showed significantly increased ROS, DNA damage, TNF-α, and IL-6. SOD was significantly decreased in severe CAP. Vitamin C significantly decreased ROS, DNA damage, TNF-α, and IL-6. Vitamin C inhibited LPS-induced ROS, DNA damage, TNF-α, IL-6, and p38 in macrophages cells. Vitamin C inhibited autophagy in LPS-induced macrophages cells. These findings indicated that severe CAP exhibited significantly increased oxidative stress, DNA damage, and proinflammatory mediator. Vitamin C mitigated oxidative stress and proinflammatory mediator suggesting a possible mechanism for vitamin C in severe CAP.

Choroidal vascularity index in patients with computer vision syndrome combined with accommodative lead.

BACKGROUND: This study aimed to investigate the choroidal vascularity index (CVI) in patients with computer vision syndrome (CVS) combined with accommodative lead. METHODS: This retrospective case-control study enrolled patients diagnosed with CVS and accommodative lead at the XXX Hospital affiliated to XXX University between July 2022 and May 2023. The control group included individuals without any ocular diseases. Ophthalmic assessments included basic visual acuity, refraction, ocular biometric parameters, and CVI. RESULTS: A total of 85 participants were included in the study, with 45 in the CVS group and 40 in the control group. The central corneal thickness of CVS group was found to be significantly thinner compared to the control group in both the right eye (532.40±30.93 vs. 545.78±19.99 µm, P=0.019) and left eye (533.96±29.57 vs. 547.56±20.39, P=0.014). In comparison to the control group, the CVS group exhibited lower CVI in the superior (0.40±0.08 vs. 0.43±0.09, P=0.001), temporal (0.40±0.08 vs. 0.44±0.10, P<0.001), inferior (0.41±0.08 vs. 0.46±0.08, P<0.001), and nasal (0.41±0.08 vs. 0.44±0.08, P=0.001) quadrants. Similar differences were observed in all four quadrants within the 1-3 mm radius, and in the temporal (P=0.004) and inferior (P=0.002) quadrants within the 1-6 mm and 3-6 mm radii (all P<0.05). CONCLUSION: Compared to individuals without ocular issues, patients with CVS and accommodative lead were found to have thinner corneal central thickness and lower CVI.

Detecting Pesticide Dodine by Displacement of Fluorescent Acridine from Cucurbit[10]uril Macrocycle.

According to a simple guest-replacement fluorescence turn-on mechanism, we constructed a fluorescent probe system based on cucurbit[10]uril (Q[10]) and protonated acridine (AD) to detect the pesticide dodine (DD). Formation of a homoternary inclusion complex AD2@Q[10] in both aqueous solution and solid state was studied by means of 1H NMR spectroscopy and X-ray crystallography. Although AD can emit strong fluorescence in aqueous solution, the homoternary inclusion complex AD2@Q[10] does not exhibit any fluorescence. Upon the addition of the pesticide DD into the aqueous solution of AD2@Q[10], the AD molecules in the Q[10] cavity are displaced by the pesticide DD, and strong fluorescence recovers. The fluorescent probe system based on Q[10] and AD provided a wide determination of DD from 0 to 4.0 × 10-5 mol·L-1 with a low limit of detection of 1.827 × 10-6 mol·L-1. The guest-replacement fluorescence turn-on mechanism is also confirmed by 1H NMR spectroscopy. Further, the fluorescent probe can directly detect DD residues in real agricultural products, and obvious fluorescence signal was observed under UV irradiation.

25-Hydroxyvitamin D3-deficiency enhances oxidative stress and corticosteroid resistance in severe asthma exacerbation.

Oxidative stress plays a significant role in exacerbation of asthma. The role of vitamin D in oxidative stress and asthma exacerbation remains unclear. We aimed to determine the relationship between vitamin D status and oxidative stress in asthma exacerbation. Severe asthma exacerbation patients with 25-hydroxyvitamin D3-deficiency (V-D deficiency) or 25-hydroxyvitamin D-sufficiency (V-D sufficiency) were enrolled. Severe asthma exacerbation with V-D-deficiency showed lower forced expiratory volume in one second (FEV1) compared to that with V-D-sufficiency. V-D-deficiency intensified ROS release and DNA damage and increased TNF-α, OGG1 and NFκB expression and NFκB phosphorylation in severe asthma exacerbation. Supplemental vitamin D3 significantly increased the rates of FEV1 change and decreased ROS and DNA damage in V-D-deficiency. Vitamin D3 inhibited LPS-induced ROS and DNA damage and were associated with a decline in TNF-α and NFκB in epithelial cells. H2O2 reduces nuclear translocation of glucocorticoid receptors in airway epithelial cell lines. V-D pretreatment enhanced the dexamethasone-induced nuclear translocation of glucocorticoid receptors in airway epithelial cell lines and monocytes from 25-hydroxyvitamin D3-deficiency asthma patients. These findings indicate that V-D deficiency aggravates oxidative stress and DNA damage, suggesting a possible mechanism for corticosteroid resistance in severe asthma exacerbation.