Trillium tschonoskii rhizome saponin improves spatial learning and memory by enhancing neurovascular restorative in ischemic rats.

Phytomedicine

School of Traditional Chinese Medicine, Capital Medical University, Beijing, China; Beijing Key Lab of TCM Collateral Disease Theory Research, Beijing, China. Electronic address:

Published: December 2024

AI Article Synopsis

  • Trillium tschonoskii rhizome saponins (TSTT) are traditionally used in folk medicine for conditions like traumatic injury and cancer, but the specific mechanisms behind its neurovascular restorative effects after ischemia are not fully understood.
  • The purpose of the study was to investigate the effectiveness of TSTT in promoting recovery in ischemic rats, particularly regarding neurovascular repair and improvements in spatial learning and memory.
  • Experimental methods included creating a permanent ischemia model in rats, administering various doses of TSTT, and using MRI, behavioral tests, and histopathological techniques to assess brain health and neuronal repair, with results showing that TSTT reduced infarction and improved brain structure and function compared to untreated controls

Article Abstract

Background: Trillium tschonoskii rhizome saponins (TSTT) has been significantly effective in treating traumatic injury, neurasthenia, cancer and inflammatory diseases as a folk medicine. However, the mechanism regarding to TSTT induced the neurovascular restorative after ischemia is without fully elucidated.

Purpose: This research was constructed to study the value of TSTT in promoting endogenous repair of neurovascular and augmenting the ability of spatial study and memory retention in ischaemic rats.

Study Design: The improvement of TSTT on cerebral infraction and perfusion was observed by magnetic resonance imaging (MRI) experiments and the molecular mechanisms were further explored.

Methods: First, rats were ligated the middle cerebral artery to construct a permanent ischaemia model, subsequently intragastric injection administrated with TSTT (120, 60, 30 mg kg) at 6 h after operation, then once a day during next 30 days. Morris water maze was applied to observe the neurobehavioral changes. Multimodal MRI sequences were performed to monitoring brain injuries as well as cerebral blood flow. Histopathological staining was employed to evaluate the morphological changes of neurons. Transmission electron microscopy (TEM) was employed to detect the neurons, vascular structure, and synapse. Immunofluorescent staining was utilized to evaluate the endogenous repair progress. The axonal growth-inhibitors and axonal guidance cues were analyzed using western blotting.

Results: Contrast to the model group, TSTT declined the infarction and elevated the parenchymal volume. Notably, treated with TSTT significantly decreased the ADC (ipsilateral/contralateral). In histopathologic examination, TSTT prominently boosted amounts of cortical and striatal nerve cells and protected ultrastructure of neurovascular unit. According with results of nuclear magnetic imaging, TSTT enhanced endogenous repair progress. Especially, TSTT treatments obviously inhibited protein levels of NogoA/NgR/RhoA/ROCK2, accompanied by increased expression of Netrin/DCC and Slit2/Robo1.

Conclusion: To sum up, our data illustrated that TSTT promoted cerebral reestablishment. The above result was in line with improving cerebral blood flow, elevated integrity of neurovascular structure, accelerating endogenous restoration and impairing the axonal growth inhibitors NogoA/NgR/RhoA/ROCK2 signaling, thereby improving poststroke learning and memory.

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Source
http://dx.doi.org/10.1016/j.phymed.2024.156096DOI Listing

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