To date, a lot of studies have been conducted to study selleck bio the distribution and expression of miRNAs under physiological conditions and after cerebral ischemia. In physiological conditions, 152 miRNAs have been detected in different nervous tissues (central and peripheral nervous tissues) of rats [15]; the results showed 30 miRNAs were specifically expressed in the nervous tissues of rats and the expression of most miRNAs varies among sites of nervous tissues. For example, in the central nervous system, miR-21 is expressed in both cortex and olfactory bulb, but the expression of several miRNAs is confined to a certain nervous tissue (miR-let-7b, miR-16, miR-22, miR-206, and miR-143 are only expressed in the olfactory bulb).

A series of miRNAs was closely related to the growth and development, differentiation, physiological function, and pathology of nervous system. These miRNAs together with their target genes were involved in some important processes of stroke including endothelial dysfunction, abnormal regulation of nervous system and blood vessels, formation of edema, cell apoptosis, inflammation and remodeling of extracellular matrix (ECM). Other studies also indicated that focal cerebral ischemia may significantly alter the transcription and translation of mRNA through the regulation of the expression of relevant miRNAs, which might be a pathophysiological mechanism underlying the stroke and PSD. These findings provide theoretical basis for the treatment of stroke and PSD.2.2. Complicated Pathogenesis of PSDThe correlation between stroke and PSD is complex and PSD is one of common complications of stroke.

At least 1/3 of patients with acute stroke develop depression [16]. Depression may increase the morbidity, disability, and mortality of stroke. In the chronic stage, the symptoms of depression may further deteriorate and finally result in recognition impairment. PSD may manifest as general emotional disturbance including anxiety, feeling of despair, and anhedonia. Studies have revealed that the pathogenesis of depression is attributed to the reduced neurogenesis and disturbance of brain plasticity. Timely use of antidepression therapy after stroke may significantly reduce the incidence of PSD. Rationale application of antidepressants may markedly improve symptoms of depression and provide neuroprotective effects to brain plasticity and neurogenesis.

Accumulating pieces of evidence have shown that selective serotonin reuptake inhibitor (SSRI) could improve the prognosis of stroke patients and reduce the incidence of PSD. Although PSD is responsive to antidepressants, few animal models GSK-3 have been established for the investigation of depression, and the molecular mechanism underlying the pathogenesis of PSD remains unclear.In recent years, some studies have been conducted to investigate the pathogenesis of PSD.