Hyperglycemia (HG) affects cellular organelle including mitochondrion in retina that diminishes mitochondrial biogenesis by downregulation of nuclear transcription factors peroxisome proliferator‐activated receptor‐γ coactivator‐1 (PGC‐1α) and mitochondrial transcription factor A (TFAM). Mitochondrial dysfunction has been linked to diabetic retinopathy (DR). Carotenoids reported to modulate mitochondrial biogenesis in HG. Aim of the study was to explore the role of lutein, oxidized lutein (purified upon UV oxidation of lutein) and drug metformin, on mitochondrial biogenesis in HG‐induced ARPE‐19 cells and rat retina. Results showed higher uptake of lutein and oxidized lutein in ARPE‐19 cells and rat retina of HG group than the control groups. Further, lutein and oxidized lutein augmented the AMPK phosphorylation and activation of mitochondrion signaling molecule TFAM (protein expression) and mRNA expression of PGC‐1α, TFAM, and nuclear respiratory factor 1 (responsible for mitochondria biogenesis) along with lowered reactive oxygen species in HG compared with control and metformin groups. Higher mRNA expression of nicotinamide adenine dinucleotide dehydrogenase subunits mt‐ND1, mt‐ND4, mt‐ND6, and cytochrome C that aid maintenance of mtDNA integrity was also evidenced. To conclude, lutein and oxidized lutein found to upsurge mitochondrial biogenesis in ARPE‐19 cells and rat retina under HG, which may be due to upregulation of AMPK phosphorylation. Finally, lutein and oxidized lutein may provide a therapeutic basis to ameliorate HG‐induced DR.

The stimulation of adenosine monophosphate‐activated protein kinase (AMPK) is a prime target to decrease the hyperglycemic condition, hence it is a lutein (L) and oxidised lutein (OXL) is a target molecule for the treatment of type II diabetes. In the current study, a plausible interaction of L and OXL with AMPK was investigated by molecular docking. In addition, the effect of L and OXL for the activation of AMPK that triggers the downstream regulator peroxisome proliferator‐activated receptor γ coactivator 1α (PGC‐1α), TFAM expression, mitochondrial DNA (mtDNA), mitochondrial biogenesis and superoxide dismutase 2 (SOD2) in high glucose treated HepG2 cells were investigated by quantitative polymerase chain reaction and Western blot analysis. Molecular docking reveals higher binding affinity of L (ΔG = −6.3 kcal/mol) and OXL (ΔG = −15.5 kcal/mol) with AMPK, compared with metformin (ΔG = −5.0 kcal/mol). The phosphorylation of AMPK increased by 1.3‐ and 1.5‐fold with L and OXL treatment, respectively, in high glucose induced HepG2 cells. The activation of PGC‐1α is significant (P < 0.05) in OXL group than L. Similarly, TFAM expression is increased with L and OXL compared with the high glucose group. Further increase in SOD2 and mtDNA, confirms the efficacy of L and OXL in restoring the mitochondrial biogenesis in high glucose induced cells through AMPK, PGC‐1α, and TFAM.

In recent years, several eco-friendly processes for the synthesis of silver nanoparticles (AgNPs) are increasing; they have tremendous applications in the field of diagnosis and therapeutic values for various diseases /disorders. In this article the green synthesis of Datura stramonium leaves extract silver nanoparticles (DS-AgNPs) was carried out and are characterized for different properties like reduction of Ag + to Ag◦, absorption maxima, functional group of secondary metabolites, crystalline structure, morphology, and size by using UV-Vis spectroscopy, fourier transform infrared spectroscopy (FITR) X-ray spectroscope (XRD), scanning electron microscopy (SEM) and atomic force microscopy (AFM) respectively. Further the effects of DS-AgNPs on WT Park TM3 SB and WI Park 25 Parkinson’s mutant Drosophila melanogaster was assessed by the Negative geotaxis assay and PINK 1 gene expression. Treatment with DS-AgNPs exhibited increased geotaxis behavior and with a positive survival percentage, finally PINK1 was found to be down regulated as the treatment concentrations increased in WI Park 25 mutant but up regulated in WT Park TM3 SB mutant PD model. Although more molecular mechanism needs to be understood, however the use of DS-AgNPs can be a promising treatment strategy for the PD.

Liposomes and other types of nanoparticles are increasingly being explored for drug delivery in a variety of diseases. There is an impetus in the field to exploit different types of ligands to functionalize nanoparticles to guide them to the diseased site. Most of this work has been conducted in the cancer field, with relatively much less information from autoimmune diseases, such as rheumatoid arthritis (RA). Furthermore, in RA, many drugs are self-administered by patients subcutaneously (SC). In this context, we have examined the attributes of liposomes functionalized with a novel joint-homing peptide (denoted ART-1) for arthritis therapy using the SC route. This peptide was previously identified following phage peptide library screening in the rat adjuvant arthritis (AA) model. Our results show a distinct effect of this peptide ligand on increasing the zeta potential of liposomes. Furthermore, liposomes injected SC into arthritic rats showed preferential homing to arthritic joints, following a migration profile in vivo similar to that of intravenously injected liposomes, except for a less steep decline after the peak. Finally, liposomal dexamethasone administered SC was more effective than the unpackaged (free) drug in suppressing arthritis progression in rats. We suggest that with suitable modifications, this SC liposomal treatment modality can be adapted for human RA therapy.