ABSTRACT
Epilepsy refers to a clinical syndrome generated by spontaneous seizures in the central nervous system. Epilepsy triggers a complex pathological process including inflammatory response and aquaporin 4 (AQP4) increase. It has been reported that AQP4 helps to enhance the immunological function of the central nervous system in pathological conditions, but the relationship between AQP4 and inflammatory cytokines is poorly understood in chronic epilepsy processes. As an inhibitor of sulfonamide carbonic anhydrase (CA), acetazolamide (AZA) may inhibit water infiltration through AQP4. In this context, pentylenetetrazole (PTZ) is used to induce the chronic epilepsy model in rats to study the chronic epilepsy effects of AQP4 inhibition on proinflammatory cytokine expression in the hippocampus and proinflammatory cytokine quantification analysis of the plasma. Based on the assumption that AQP4 regulates proinflammatory cytokine expression, this article aims to demonstrate this effect in chronic epilepsy of rats. Rats were divided into four groups and were treated with different drugs: saline (Control), acetazolamide (AZA), pentylenetetrazole (PTZ), and pentylenetetrazole plus acetazolamide (PTZ+AZA). The data showed that seizures increased proinflammatory cytokine expression and that AZA significantly inhibited AQP4 expression. Overall, the results suggested that AQP4 inhibition could weaken excitotoxicity in epileptogenesis by reducing proinflammatory cytokines in the hippocampus. The findings provide a new insight into the involvement of cerebral edema insult and proinflammatory cytokines in the process of chronic epilepsy.
Subject(s)
Acetazolamide/pharmacology , Aquaporin 4/antagonists & inhibitors , Cytokines/biosynthesis , Epilepsy/chemically induced , Epilepsy/metabolism , Hippocampus/metabolism , Microvessels/metabolism , Animals , Aquaporin 4/blood , Aquaporin 4/genetics , Aquaporin 4/metabolism , Chronic Disease , Epilepsy/blood , Epilepsy/genetics , Hippocampus/blood supply , Hippocampus/pathology , Kindling, Neurologic/genetics , Microvessels/pathology , Pentylenetetrazole , RNA, Messenger/genetics , RNA, Messenger/metabolism , Rats, Sprague-Dawley , Up-Regulation/drug effects , Up-Regulation/geneticsABSTRACT
Broussonetia papyrifera is an important native tree species with high economic value in southwest China. Its resources are drastically reduced because of over-harvesting and habitat fragmentation. In this study, 17 natural populations of B. papyrifera were analyzed using inter-simple sequence repeat (ISSR) markers to assess the genetic diversity and population structure. In total, 100 bands were obtained from 16 ISSR primers. The B. papyrifera populations showed relatively high genetic diversity at the species level [percentage of polymorphic bands (PPB): 96%; Nei's genetic diversity (HE): 0.3074; Shannon's information index (I): 0.4617], while the genetic diversity at the population level was relatively low (PPB: 53.2%; HE: 0.1826; I: 0.2735). Relatively high level of genetic differentiation among populations (41%) was disclosed by analysis of molecular variance, which agrees with the Nei's genetic diversity statistics (40.59%) and Shannon's information measure (40.76%). Gene flow among populations (NM) was only 0.7318. A significant correlation was observed between genetic and geographic distance among the studied populations (r=0.2948). We conjectured that the genetic diversity of B. papyrifera resulted from human disturbance, habitat fragmentation, small effective population size, and geographic barrier. Given the high genetic differentiation among populations, some utilization and conservation strategies were proposed. This study provides a reference for the sustainable use of the species in southwest China.