beta-escin and Brain-Injuries

Studies in 142 accident victims with severe craniocerebral trauma showed that the intravenous application of sodium escinate over several days considerably reduced the dangerous rise in intracranial pressure and also the total mortality in comparison with corticosteroid therapy alone. Both groups, each of 71 patients, were adjusted from an initial intraventricular pressure of 500--250 mm H2O to the same basic pressure of 150 mm H2O hydrostatically. In the same way, sodium escinate shortened the duration of unconsciousness. The renal function in patients was good. Follow-up examinations at least 2 to a maximum of 3.5 years after the accident and treatment showed a significantly higher rehabilitation rate in the sodium escinate group.

Topics: Adrenal Cortex Hormones; Blood Transfusion; Brain Edema; Brain Injuries; Escin; Female; Humans; Injections, Intravenous; Intracranial Pressure; Male; Saponins; Vitamin B Complex

Hyperactivity of HPA axis results in intestinal dysfunction, which may play a role in brain injury caused by ischemic stroke (IS). Escin shows a neuroprotective effect but it may not penetrate blood brain barrier (BBB). Previous work in our laboratory showed that escin ameliorated intestinal injury in animals. The aim of this study is to investigate whether escin attenuates brain injury by improving intestinal dysfunction in middle cerebral artery occlusion (MCAO) rats, to mimic IS. MCAO rats and lipopolysaccharides (LPS)-induced Caco-2 cells were used to evaluate the effects of escin in vivo and in vitro. The results showed that escin could not penetrate BBB but reduced brain infarct volume, improved neurological function, inhibited neuroinflammation, ameliorated intestinal dysfunction and tissue integrity by increasing the expression of the tight junction protein in vivo and in vitro. Escin reduced the increased corticosterone and endotoxin level in blood of MCAO rats, regulated GR/p38 MAPK/NF-κB signaling pathway in ileal tissue and LPS/TLR4/NF-κB signaling pathway in ischemic brain tissue. These findings suggest that escin could attenuate ischemic brain injury by improving intestinal dysfunction, and it may be a promising way to protect brain injury by protecting intestine, instead of targeting the brain directly after IS.

Topics: Animals; Brain Injuries; Brain Ischemia; Brain-Gut Axis; Caco-2 Cells; Escin; Gastrointestinal Diseases; Humans; Hypothalamo-Hypophyseal System; Infarction, Middle Cerebral Artery; Intestinal Diseases; Ischemic Stroke; Lipopolysaccharides; NF-kappa B; Pituitary-Adrenal System; Rats; Reperfusion Injury; Stroke

To investigate the inhibiting effect of beta-Aescin on nuclear factor-kappaB (NF-kappaB) activation and the expression of tumor necrosis factor-alpha (TNF-alpha) protein after traumatic brain injury (TBI) in the rat brain, 62 SD rats were subjected to lateral cortical impact injury caused by a free-falling object and divided randomly into four groups: (1) sham operated (Group A); (2) injured (Group B); (3) beta-Aescin treatment (Group C); (4) pyrrolidine dithocarbamate (PDTC) treatment (Group D). Beta-Aescin was administered in Group C and PDTC treated in Group D immediately after injury. A series of brain samples were obtained directly 6 h, 24 h and 3 d respectively after trauma in four groups. NF-kappaB activation was examined by Electrophoretic Mobility Shift Assay (EMSA); the levels of TNF-alpha protein were measured by radio-immunoassay (RIA); the water content of rat brain was measured and pathomorphological observation was carried out. NF-kappaB activation, the levels of TNF-alpha protein and the water content of rat brain were significantly increased (P<0.01) following TBI in rats. Compared with Group B, NF-kappaB activation (P<0.01), the levels of TNF-alpha protein (P<0.01) and the water content of brain (P<0.05) began to decrease obviously after injury in Groups C and D. Beta-Aescin could dramatically inhibit NF-kappaB activation and the expression of TNF-alpha protein in the rat brain, alleviate rat brain edema, and that could partially be the molecular mechanism by which beta-Aescin attenuates traumatic brain edema.

Topics: Animals; Body Water; Brain Edema; Brain Injuries; Escin; NF-kappa B; Pyrrolidines; Rats; Rats, Sprague-Dawley; Thiocarbamates; Treatment Outcome; Tumor Necrosis Factor-alpha

Topics: Brain Edema; Brain Injuries; Dexamethasone; Escin; Humans; Hypertonic Solutions; Intracranial Pressure

The treatment and follow-up treatment of head injuries patients requires a drug, which will combat the development of cerebral edema by acting on the blood-brain barrier and restoring the normal function of endothelium and basal membrane. Such a drug should be easy to administer and free from serious side-effects, so that it can be employed for follow-up treatment by the general practitioner without the necessity of hospital facilities (EEG, CT, etc.). In a series of 3557 patients with head injuries Reparil has shown to be a suitable drug in treatment and follow-up treatment of posttraumatic brain edema. In follow-up treatment close medical supervision is essential so that any complications such as intracranial haematomas can be recognized in good time. This applies in particular to patients in high risk groups (advanced age, presence of concurrent diseases, in particular metabolic and circulatory disturbances).

Topics: Adolescent; Adult; Aged; Blood-Brain Barrier; Brain Edema; Brain Injuries; Child; Child, Preschool; Escin; Female; Humans; Infant; Intracranial Pressure; Male; Middle Aged; Tomography, X-Ray Computed

Topics: Brain Edema; Brain Injuries; Dexamethasone; Escin; First Aid; Home Nursing; Hospitalization; Humans; Physicians, Family; Skull

Topics: Aprotinin; Brain Edema; Brain Injuries; Dihydroergotamine; Diuretics; Escin; Glucocorticoids; Humans; Parasympatholytics; Trephining

Topics: Adolescent; Adult; Aged; Brain Edema; Brain Injuries; Child; Child, Preschool; Dexamethasone; Diuretics; Escin; Female; Humans; Infant; Male; Mannitol; Middle Aged; Parasympatholytics; Sorbitol

The aim of this paper is to contrast new results obtained on the activities of lysosomal proteases in the brain of traumatized animals with the previously held opinions concerning the development of post-traumatic brain oedema. Two hours after a standardized head injury in the cat, acid and neutral proteases were determined in the brain homogenate. Total as well as free activity, especially of the neutral proteases, were markedly increased after head injury, a circumstance indicating the important role of lysosomes in the development of post-traumatic brain oedema. It is postulated that not hypoxia alone, but primary or secondary disturbance of lysosomal function is the predominant factor in the development of brain oedema. Release of enzymes -- especially proteases -- causes irreversibility of initial vascular oedema by autolysis of cellular structures.

Topics: Animals; Brain Edema; Brain Injuries; Cats; Cortisone; Diuretics; Escin; Lysosomes; Peptide Hydrolases

Topics: Brain; Brain Concussion; Brain Injuries; Drug Combinations; Escin; Humans; Plant Extracts; Thiamine