TY - JOUR
AB - Gastrodia elata (GE) Blume has been widely used for thousands of years to treat various central and peripheral nervous disorders. P‑hydroxybenzaldehyde (PHBA) is a chemical component of GE. However, its role and mechanism in transient focal cerebral ischemia remain unclear. The present study aimed to investigate the protective effect of PHBA on middle cerebral artery occlusion (MCAO) rats. A total of 56 Sprague‑Dawley male rats were randomly divided into control, model, PHBA‑high dose (PHBA‑H) and PHBA‑low dose (PHBA‑L) groups. The MCAO injury model was replicated in all rats except for the control group. In the control group, only the right common carotid artery was isolated without embolization. After treatment with PHBA, the protective effects (neurological deficit score, cerebral index, weight and cerebral infarct) were analyzed. Western blotting was performed to estimate the protein levels of Bcl‑2, Bax and Caspase‑3. Apoptotic cells were detected using hematoxylin‑eosin staining and TUNEL immunofluorescence assay. Mitochondrial oxidative stress indicators, including reactive oxygen species (ROS), malondialdehyde (MDA) and total superoxide dismutase (T‑SOD), while dysfunction indicators, including mitochondrial permeability transition pore (MPTP), ATP and cytochrome C oxidase, were measured using commercial kits. The ultrastructure of mitochondria was observed under an electron microscope. Once the model was successful established, the rats in the MCAO group suffered neurological damage (P<0.001), increased cerebral index (P<0.001), decreased body weight (P<0.001) and had severe cerebral infarction (P<0.001). Moreover, the number of apoptotic cells and the levels of ROS (P<0.001) and MDA (P<0.05) in mitochondria and the protein levels of Bax (P<0.001) and cleaved caspase‑3 (P<0.001) were increased. The activities of T‑SOD (P<0.001) and cytochrome C oxidase (P<0.001) in the mitochondria, ATP content (P<0.05) and Bcl‑2 protein level (P<0.001) decreased, MPTP was stimulated to open and mitochondrial structures were damaged (P<0.001). PHBA treatment resulted in a decrease of the neurological deficit score (PHBA‑H 24 h, P<0.001; PHBA‑H 6 h and PHBA‑L 24 h, P<0.01; PHBA‑L 6 h, P<0.05), apoptotic cell number (P<0.001), mitochondrial ROS (P<0.001) and MPTP opening (P<0.001), Bax (P<0.01, P<0.001) and cleaved caspase‑3 protein expression (P<0.001) in rats. And the expression of Bcl‑2 protein (P<0.001) was increased. In addition, the cerebral index (P<0.05), weight loss (P<0.05), infarction rate (P<0.01) and MDA content (P<0.001) were decrease in the PHBA‑H group. The level of ATP (P<0.05) and cytochrome C oxidase (P<0.05) and T‑SOD activity (P<0.05) of PHBA‑H group rats increased, but no significant difference was observed in the PHBA‑L group. Overall, PHBA had a protective effect on transient focal cerebral ischemia in normal rats, regulated the expression of Bcl‑2, Bax and cleaved caspase‑3 proteins and improved the oxidative stress and dysfunction of mitochondria.
AD - Yunnan Key Laboratory of Dai and Yi Medicines, Yunnan University of Chinese Medicine, Kunming, Yunnan 650500, P.R. China
AU - Xiao,Tian
AU - Yang,Liping
AU - Chen,Pu
AU - Duan,Xiaohua
DA - 2022/12/01
DO - 10.3892/etm.2022.11652
IS - 6
JO - Exp Ther Med
KW - P‑hydroxybenzaldehyde
Gastrodia elata Blume
ischemic stroke
middle cerebral artery occlusion
Bcl‑2/Bax protein
caspase‑3 protein
oxidative stress
dysfunction of mitochondria
PY - 2022
SN - 1792-0981
1792-1015
SP - 716
ST - Para‑hydroxybenzaldehyde against transient focal cerebral ischemia in rats via mitochondrial preservation
T2 - Experimental and Therapeutic Medicine
TI - Para‑hydroxybenzaldehyde against transient focal cerebral ischemia in rats via mitochondrial preservation
UR - https://doi.org/10.3892/etm.2022.11652
VL - 24
ER -