Dry eye disease (DED) represents a prevalent visual ailment, defined by insufficient wetting and lubrication of the ocular surface. The principal management strategy for dry eye involves the application of artificial tear solutions to mitigate eye discomfort. Moreover, immune-modulating agents such as cyclosporine A and tacrolimus (FK506) are employed in the therapeutic regimen for this condition. These drugs regulate the immune response and reduce ocular inflammation. Tacrolimus (TAC) is 10-100 times more effective than cyclosporine and has a better safety profile. Nevertheless, the modest aqueous solubility and substantial molecular size of TAC present obstacles to its efficient administration to the eye. Consequently, a range of TAC formulations including ointments, micelles, liposomes, and nanocarriers are under exploration to enhance ocular delivery. Findings from this investigation indicated that TAC impedes the secretion of pro-inflammatory cytokines and dampens immune activity by restraining the activation of T and B lymphocytes. Furthermore, TAC elevates goblet cell populations in the conjunctiva, pivotal for mucin production and the preservation of ocular surface integrity. Additionally, using TAC-loaded liposomes can further enhance its therapeutic efficacy by improving ocular bioavailability. Furthermore, 0.03% TAC eye drops applied directly to the eye successfully improve tear film stability and the health of the eye’s surface in patients with DED. Overall, TAC has shown promising effects in treating DED by reducing inflammation and improving tear secretion in experimental and clinical studies. However, more studies are needed to fully understand the mechanism of action and long-term effects of TAC on DED.

Parkinson’s disease (PD) is a neurodegenerative disorder characterized by the loss of dopaminergic neurons in the substantia nigra, leading to various motor and non-motor symptoms. Several cellular and molecular mechanisms such as alpha-synuclein (α-syn) accumulation, mitochondrial dysfunction, oxidative stress, and neuroinflammation are involved in the pathogenesis of this disease. MicroRNAs (miRNAs) play important roles in post-transcriptional gene regulation. They are typically about 21-25 nucleotides in length and are involved in the regulation of gene expression by binding to the messenger RNA (mRNA) molecules. miRNAs like miR-221 play important roles in various biological processes, including development, cell proliferation, differentiation, and apoptosis. miR-221 is also implicated in promoting neuronal survival against oxidative stress and in promoting neurite outgrowth and neuronal differentiation. Additionally, the role of miR-221 in PD has been investigated in several studies. According to the results of this study; 1) miR-221 protects against oxidative stress in 6-hydroxydopamine-induced PC12 cells; 2) miR-221 prevents Bax/caspase-3 signaling activation by stopping Bim; 3) miR-221 has moderate predictive power for PD; 4) miR-221 directly targets PTEN, and PTEN over-expression eliminates the protective action of miR-221 on p-AKT expression in PC12 cells; 5) miRNA-221, by manipulating the Akt signaling pathway, performs in controlling cell viability and apoptosis in PD. This review study suggests that miR-221 has the potential to be used as a clinical biomarker for PD diagnosis and stage assignment.