Search

Salvianolic acid A (SalA), a bioactive compound extracted from Salvia miltiorrhiza, has garnered considerable interest for its potential in ameliorating the post-stroke neuroinflammation. This review delineates the possible molecular underpinnings of anti-inflammatory and neuroprotective roles of SalA, offering a comprehensive analysis of its therapeutic efficacy in preclinical studies of ischemic stroke. We explore the intricate interplay between post-stroke neuroinflammation and the modulatory effects of SalA on pro-inflammatory cytokines, inflammatory signaling pathways, the peripheral immune cell infiltration through blood-brain barrier disruption, and endothelial cell function. The pharmacokinetic profiles of SalA in the context of stroke, characterized by enhanced cerebral penetration post-ischemia, makes it particularly suitable as a therapeutic agent. Preliminary clinical findings have demonstrated that salvianolic acids (SA) has a positive impact on cerebral perfusion and neurological deficits in stroke patients, warranting further investigation. This review emphasizes SalA as a potential anti-inflammatory agent for the advancement of innovative therapeutic approaches in the treatment of ischemic stroke.

Storm-induced episodic sediment redistribution in coastal systems can reshape geomorphic bodies, disrupt ecosystems, and cause economic damage. However, cold-wave-storm-induced hydrodynamic changes and residual sediment transport in large, exposed subaqueous deltas, such as the Yangtze Delta, are poorly understood because it is typically expensive and difficult to obtain systematic field data in open coast settings during storm events. We conducted a successful field survey of waves, currents, changes in water depth, and turbidity at a station (time-averaged water depth of 20 m) in the offshore subaqueous Yangtze Delta over 10 days during winter, covering two storms and two fair-weather periods. During the storm events, strong northerly winds drove southward longshore currents (~0.2 m/s) and resulted in increased wave height and sediment resuspension, thereby leading to massive southward sediment transport. In contrast, both southward and northward transports were limited during the fair-weather periods. A better understanding of the storm-induced sediment transport can be obtained by using an approximately half-day lag in sediment transport behind wind force, given the time needed to form waves and longshore drift, the inertia of water motion, and the slow settling velocity of fine-grained sediment. Our results directly support previous findings of southward sediment transport from the Yangtze Delta during winter, which is deposited in the Zhejiang–Fujian mud belt in the inner shelf of the East China Sea. In addition, the southward sediment transport from the Yangtze Delta occurs mainly during episodic storm events, rather than during the winter monsoon, and winter storms dominate over typhoons in driving southward sediment transport from the delta. This study highlights the importance of storms, especially during winter storms, in coastal sediment redistribution, which is of particular significance when considering the projected increase in storm intensity with global warming.

Following a cerebral ischemic event, substantial alterations in both cellular and molecular activities occur due to ischemia-induced cerebral pathology. Mounting evidence indicates that the robust recruitment of immune cells plays a central role in the acute stage of stroke. Infiltrating peripheral immune cells and resident microglia mediate neuronal cell death and blood-brain barrier disruption by releasing inflammation-associated molecules. Nevertheless, profound immunological effects in the context of the subacute and chronic recovery phase of stroke have received little attention. Early attempts to curtail the infiltration of immune cells were effective in mitigating brain injury in experimental stroke studies but failed to exert beneficial effects in clinical trials. Neural tissue damage repair processes include angiogenesis, neurogenesis, and synaptic remodeling, etc. Post-stroke inflammatory cells can adopt divergent phenotypes that influence the aforementioned biological processes in both endothelial and neural stem cells by either alleviating acute inflammatory responses or secreting a variety of growth factors, which are substantially involved in the process of angiogenesis and neurogenesis. To better understand the multiple roles of immune cells in neural tissue repair processes post stroke, we review what is known and unknown regarding the role of immune cells in angiogenesis, neurogenesis, and neuronal remodeling. A comprehensive understanding of these inflammatory mechanisms may help identify potential targets for the development of novel immunoregulatory therapeutic strategies that ameliorate complications and improve functional rehabilitation after stroke.