ABSTRACT
ObjectiveTo investigate the effect of Rehmanniae Radix Praeparata on neurological function injury in ischemic stroke rats and explore its mechanism. MethodMale SD rats were randomized into sham operation， model， low- and high -dose （3.5 g·kg-1 and 7 g·kg-1） Rehmannia Radix Praeparata， and nimodipine （0.01 g·kg-1） groups. The rat model of middle cerebral artery occlusion （MCAO） was established with the modified suture occlusion method. Zea-Longa 5-point scoring was employed to evaluate the neurological function of rats. The cerebral infarction volume was detected by 2，3，5-triphenyltetrazolium chloride （TTC） staining. Hematoxylin-eosin staining and Nissl staining were employed to observe the morphology and damage of the brain tissue. Meanwhile， the serum levels of lactate dehydrogenase （LDH）， oxidative stress-related indicators superoxide dismutase （SOD）， glutathione peroxidase 4 （GPX4）， and malondialdehyde （MDA）， and the iron （Fe） content in the brain tissue were determined. To explore the mechanism of Rehmanniae Radix Preparata in mitigating the neurological damage in ischemic stroke rats， Western blotting was employed to determine the expression levels of proteins in the ischemic brain tissue. The autophagy-associated proteins included autophagy effector （beclin-1）， microtubule-associated protein light chain 3 （LC3B）， and ubiquitin-binding protein p62 （p62）. The ferroptosis-associated proteins included transferrin （TF）， transferrin receptor 1 （TFR1）， ferritin heavy chain 1 （FTH1）， and ferropotin （FPN1）. The neurological function injury-associated proteins included brain-derived neurotrophic factor （BDNF） and tyrosine kinase receptor B （TrkB）. ResultCompared with the sham operation group， the model group showed increased neurological function score， cerebral infarction volume， and appearance of nuclear pyknosis and vacuole of cells in the cerebral cortex. In addition， the model group presented elevated levels of LDH， MDA， and Fe （P<0.01） and lowered levels of SOD and GPX4 （P<0.01）. Compared with the model group， Rehmanniae Radix Praeparata decreased the content of LDH， MDA， and Fe （P<0.05， P<0.01） and elevated the levels of SOD and GPX4 （P<0.05， P<0.01）. Compared with the sham operation group， the modeling promoted the expression of beclin-1，LC3B Ⅱ/Ⅰ， TF， and TFR1 and inhibited the expression of p62， FTH1， FPN1， BDNF， and TrkB （P<0.01）. The expression levels of these proteins were recovered after the treatment with Rehmanniae Radix Praeparata. ConclusionRehmanniae Radix Praeparata may inhibit ferroptosis and improve the neurological function in ischemic stroke rats by down-regulating the autophagy level in the brain tissue.
ABSTRACT
Malignant cerebral edema can lead to increased intracranial pressure, rapid deterioration of neurological function, and even the formation of cerebral hernia. It has the characteristics of high mortality and disability rates, and is a common cause of poor prognosis in patients with acute massive cerebral infarction. Early decompressive craniectomy can effectively improve the neurological outcomes of patients with malignant cerebral edema. Therefore, early prediction of malignant cerebral edema is crucial. This article reviews the formation mechanism and related imaging manifestations of malignant cerebral edema, in order to provide reference and assistance for the early diagnosis and reasonable treatment of malignant cerebral edema after massive cerebral infarction.
ABSTRACT
Glymphatic system is a fluid transport and material clearance system found in recent years. It promotes the flow and exchange of cerebrospinal fluid and interstitial fluid, remove metabolic waste, and maintain the stability of the internal environment of the brain through the perivascular space and aquaporin 4 on astrocytes. Recent studies have shown that the glymphatic system plays an important role in the intake and discharge of the fluid in brain, and the changes of glymphatic system may be an important reason for brain edema after ischemic stroke. This article reviews the pathophysiological mechanism and related therapeutic targets of glymphatic system in the formation of cerebral edema after ischemic stroke, in order to provide new ideas for the treatment of cerebral edema after ischemic stroke.