Current topics in medicinal chemistry · 2026
Total Alkaloids of Yanhusuo Attenuate Chronic Cerebral Hypoperfusion-Induced Brain Injury: Mechanisms and Neuroprotection.
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Tian Bing, Huang Shuming, Song Yutong, Bai Biwei, Fang Jing, Sun Xiangming, Li Chenxue, Yang Yue, Li Wenlan
Аннотация
INTRODUCTION: Rhizoma Corydalis, which contains alkaloids as its main active moieties, is widely used in the treatment of cerebrovascular disorders. The present study aimed to investigate the neuroprotective effects and mechanisms of the total alkaloid from Yanhusuo (YHTA) against chronic cerebral hypoperfusion (CCH).
METHODS: Sixty Sprague-Dawley (SD) rats were randomly divided into sham, model, YHTA lowdose, medium-dose, high-dose, and nimodipine positive group (n=10). A CCH model was established by performing bilateral common carotid artery occlusion. Cognitive function was assessed using behavioral tests, and neuronal morphological alterations were analyzed by histopathology. Immunohistochemistry was used to assess microvessel density and the protein expression of HIF- 1α, VEGF, and VEGFR-2. Neuronal apoptosis was detected by TUNEL assay. The protein levels of HIF-1α, VEGF, VEGFR-2, Bax, and Bcl-2 were measured by Western blotting.
RESULTS: YHTA treatment ameliorated CCH-induced cognitive impairment, alleviated neuronal damage, and increased the number of surviving neurons. All doses of YHTA inhibited neuronal apoptosis, which was associated with the upregulation of Bcl-2 and downregulation of Bax expression. Furthermore, YHTA promoted cerebral angiogenesis and upregulated the expression of HIF- 1α, VEGF, and VEGFR-2 proteins.
DISCUSSION: These results provide a pharmacological basis for the clinical application of Corydalis in cerebrovascular diseases and identify YHTA as a multi-target agent against vascular cognitive impairment and hypoperfusion-related neurodegeneration.
CONCLUSION: YHTA protects against nerve damage caused by CCH in the hippocampus. The mechanism may involve activation of the HIF-1α/VEGF/VEGFR-2 pathway, modulating the expression of apoptosis-related proteins Bcl-2 and Bax, and inhibiting nerve cell apoptosis, thereby promoting the generation of microvessels in brain tissue, improving blood flow supply, accelerating the repair of neurons, and playing a role in neuroprotection.
METHODS: Sixty Sprague-Dawley (SD) rats were randomly divided into sham, model, YHTA lowdose, medium-dose, high-dose, and nimodipine positive group (n=10). A CCH model was established by performing bilateral common carotid artery occlusion. Cognitive function was assessed using behavioral tests, and neuronal morphological alterations were analyzed by histopathology. Immunohistochemistry was used to assess microvessel density and the protein expression of HIF- 1α, VEGF, and VEGFR-2. Neuronal apoptosis was detected by TUNEL assay. The protein levels of HIF-1α, VEGF, VEGFR-2, Bax, and Bcl-2 were measured by Western blotting.
RESULTS: YHTA treatment ameliorated CCH-induced cognitive impairment, alleviated neuronal damage, and increased the number of surviving neurons. All doses of YHTA inhibited neuronal apoptosis, which was associated with the upregulation of Bcl-2 and downregulation of Bax expression. Furthermore, YHTA promoted cerebral angiogenesis and upregulated the expression of HIF- 1α, VEGF, and VEGFR-2 proteins.
DISCUSSION: These results provide a pharmacological basis for the clinical application of Corydalis in cerebrovascular diseases and identify YHTA as a multi-target agent against vascular cognitive impairment and hypoperfusion-related neurodegeneration.
CONCLUSION: YHTA protects against nerve damage caused by CCH in the hippocampus. The mechanism may involve activation of the HIF-1α/VEGF/VEGFR-2 pathway, modulating the expression of apoptosis-related proteins Bcl-2 and Bax, and inhibiting nerve cell apoptosis, thereby promoting the generation of microvessels in brain tissue, improving blood flow supply, accelerating the repair of neurons, and playing a role in neuroprotection.