Journal of ethnopharmacology · 2020
In vitro cultured calculus bovis attenuates cerebral ischaemia-reperfusion injury by inhibiting neuronal apoptosis and protecting mitochondrial function in rats.
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Lu Feibiao, Wang Lingfeng, Chen Yanyue, Zhong Xiaoming, Huang Zhen
Аннотация
ETHNOPHARMACOLOGICAL RELEVANCE: In vitro cultured calculus bovis (ICCB), which is produced based on the formation mechanism of bovine gallstones, is used to replace the natural bezoar. It has been used in the clinic to treat brain diseases, including stroke, Alzheimer's disease and depression.
AIM OF STUDY: ICCB is used to treat encephalopathy in the clinic. We explored the effects of ICCB on cerebral ischaemia-reperfusion injury (CIRI) and the potential associated mechanisms.
MATERIALS AND METHODS: Rats were subjected to middle cerebral artery occlusion for 90 min, followed by 24 h of reperfusion, after being given different concentrations of ICCB once a day for 3 days. Subsequently, the neurological scores, brain oedema and volume of cerebral infarction were measured, and the histopathological changes in the cortex neurons were observed by haematoxylin and eosin staining (H&E). Apoptosis was determined by terminal deoxynucleotidyl transferase-mediated dUTP nick end labelling (TUNEL). Ultrastructural changes in the mitochondria of the cortex were assessed by transmission electron microscopy (TEM). The apoptosis-related proteins Bax, Bcl-2, caspase-9, caspase-3, Mito-Cyt C and Cyto-Cyt C were detected by Western blotting.
RESULTS: Compared with those in the control group, the neurological scores, the volumes of cerebral infarction, and the brain water contents were significantly decreased in the ICCB groups at doses of 50 and 100 mg/kg. The ICCB treatment effectively decreased the neuronal apoptosis resulting from the CIRI-induced neuron injury. In addition, the histopathological damage and the mitochondria ultrastructure injury were partially improved in the CIRI rats after ICCB treatment. Western blotting analysis indicated that ICCB significantly decreased the expression of Bax, caspase-9, caspase-3 and Cyto-Cyt C protein levels while increasing the expression of Bcl-2 and Mito-Cyt C protein levels.
CONCLUSION: The ICCB protected against CIRI by suppressing the mitochondria-mediated apoptotic signalling pathway.
AIM OF STUDY: ICCB is used to treat encephalopathy in the clinic. We explored the effects of ICCB on cerebral ischaemia-reperfusion injury (CIRI) and the potential associated mechanisms.
MATERIALS AND METHODS: Rats were subjected to middle cerebral artery occlusion for 90 min, followed by 24 h of reperfusion, after being given different concentrations of ICCB once a day for 3 days. Subsequently, the neurological scores, brain oedema and volume of cerebral infarction were measured, and the histopathological changes in the cortex neurons were observed by haematoxylin and eosin staining (H&E). Apoptosis was determined by terminal deoxynucleotidyl transferase-mediated dUTP nick end labelling (TUNEL). Ultrastructural changes in the mitochondria of the cortex were assessed by transmission electron microscopy (TEM). The apoptosis-related proteins Bax, Bcl-2, caspase-9, caspase-3, Mito-Cyt C and Cyto-Cyt C were detected by Western blotting.
RESULTS: Compared with those in the control group, the neurological scores, the volumes of cerebral infarction, and the brain water contents were significantly decreased in the ICCB groups at doses of 50 and 100 mg/kg. The ICCB treatment effectively decreased the neuronal apoptosis resulting from the CIRI-induced neuron injury. In addition, the histopathological damage and the mitochondria ultrastructure injury were partially improved in the CIRI rats after ICCB treatment. Western blotting analysis indicated that ICCB significantly decreased the expression of Bax, caspase-9, caspase-3 and Cyto-Cyt C protein levels while increasing the expression of Bcl-2 and Mito-Cyt C protein levels.
CONCLUSION: The ICCB protected against CIRI by suppressing the mitochondria-mediated apoptotic signalling pathway.