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Aim To study the neuroprotective effects of Herba siegesbeckiae extract on cerebral ischemia/ reperfusion rats and its mechanism. Methods Sixty SD rats were randomly divided into model group, low, middle and high dose groups of Herba siegesbeckiae, and Sham operation group, and the drug was given continuously for seven days. The degree of neurologic impairment was evaluated by mNSS, and the infarct volume was measured by MRI. The number of Nissl-posi- tive cells was detected by Nissl staining, and the apop- tosis was accessed by Tunel staining. Furthermore, the expression of Bax, Bcl-2 and NeuN was observed by Western blot, and the expression of NeuN was detected by immunofluorescence staining. The expression of IL- 1β, TNF-α and IL-6 mRNA was performed by RT- qPCR. Results The mNSS score and the volume of ischemic cerebral infarction in the model group were significantly increased, and Herba siegesbeckiae extract treatment significantly decreased the mNSS score and infarct volume (P<0.05, P<0.01). Herba siegesbeckiae extract could increase the number of Nissl-pos- itive cells and the expression of NeuN (P<0.01), and reduce the number of Tunel-positive cells (P<0.01). Western blot showed that Herba siegesbeckiae extract inhibited the expression of Bax, increased Bcl-2 and NeuN in ischemic brain tissue (P<0.01). RT-qPCR showed that Herba siegesbeckiae extract inhibited the expression of IL-1 β, TNF-α and IL-6 mRNA in the is-chemic brain tissue (P<0.01). Conclusions Herba siegesbeckiae extract can reduce the cerebral infarction volume, improve the neurological function damage, inhibit the apoptosis of nerve cells and the expression of inflammatory factors and promote the expression of NeuN, there by exerting protective effects on MCAO rats.
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Aim To investigate the neuroprotective effect of prophylactic administration of salidroside (Sal) on MCAO rats. Methods A total of 52 SD adult male rats were randomly divided into sham operation group (Sham), model group (MCAO) and salidroside pre-administration group (MCAO + Sal). The dose of Sal was 50 mg·kg
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Aim To develop a ultra-high performance liquid chromatography electrospray-ionization tandem mass spectrometry ( UPLC-MS/MS ) method for the simultaneous determination of salidroside derivative pOBz in rat plasma and brain tissue, and to study the pharmacokinetic profile and penetration of the blood-brain barrier in rats after a single dose intravenous administration of pOBz. Methods SD rats were administered pOBz at a dose of 50 mg • kg
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Aim To study the effect of salidroside (SAL) on cerebral vascular endothelial cells of rats with ischemic brain injury and its mechanism of action. Methods Twenty-four healthy adult SD male rats were prepared by bolt plugging method to prepare MCAO models,and randomly divided into sham surgery group ( Sham ) , model group ( MCAO ) , and SAL administration group (MCAO + SAL) ,and the concentration of SAL was 50 mg • kg ~ , with a continuous administration for six days. Western blot was used to detect the protein expression of ICAM-1, VCAM-1 , E-se-lectin,and P-selectin in injured brain tissue of rats. In vitro cell experiments using HUVECs were subjected to different concentrations of salidroside (0. 1,1,10 jjunol • L ) and LPS (100
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Aim To study the neuroprotective effect of p-benzoyl salidroside (pOBz), a derivative of salidroside, on MCAO model rats.Methods ( 1 ) Thirty healthy adult male SD rats were randomly divided into Sham group, MCAO group and MCAO + pOBz group (25, 50, 1(X) mg • kg"1).MCAO model was made by suture-embolus method.The rats were scored for neurological function impairment and weighed every day.pOBz was intraperitoneally injected and administered continuously for two days after preparation of MCAO model.The cerebral infarction volume of rats was detected by MRI.( 2 ) Twenty-four healthy adult male SD rats were randomly divided into Sham group, MCAO group, MCAO + pOBz group (50 mg • kg"1 ) and MCAO + Sal group (50 mg • kg 1 ).The model was made by the suture-embolus method.pOBz was in-traperitoneally injected and administered continuously for one day.Western blot was used to detect the ex pression of NeuN, EGR1 , Bcl-2 and Bax.(3) Eighteen healthy adult male SD rats were randomly divided j j into Sham group, MCAO group and MCAO + pOBz group ( 50 mg • kg 1 ).Administration continued for 2 days.Immunofluorescence staining was used to detect the expression of NeuN.Results Intraperitoneal injection of pOBz for 2 days could reduce the cerebral infarction volume of MCAO rats, improve neurological impairment and increase the expression of NeuN and EGR1 , and the effect was better than that of Sal.pOBz improved Bcl-2/Bax in brain tissues of MCAO rats to the same extent as Sal did.Conclusions pOBz can reduce the volume of cerebral infarction in MCAO rats and has better neuroprotective effect than that of salidroside.
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Aim To investigate the neuroprotective effect and mechanism of salidroside (Sal) on rats with permanent middle cerebral artery occlusion model (pMCAO) by regulating the PI3 K/AKT signaling pathway. Methods A total of 80 healthy adult SPF male SD rats were randomly divided into sham operation group (sham group), model group (pMCAO group), drug administration group (pMCAO + Sal group) and inhibitor group (pMCAO + Sal + YL group). After the pMCAO model rats were prepared by the line bolt method, salidroside (50 mg · kg
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Aim To study the neuroprotective effect of rhubarb extract on MCAO model rats and explore its mechanism of action. Methods Forty-five SPF male Sprague-Dawley rats were randomly divided into sham group, MCAO group, and MCAO + rhubarb group. MCAO model was prepared by silk plug method, and rhubarb extract was administered at a concentration of 200 mg · kg
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Aim To explore the effect of Pien Tze Huang (PZH) on inhibiting HepG2 cells via regulating ANXA1/VEGF signaling pathway and the underlying mechanism. Methods HepG2 cells were treated with different concentrations (1, 1 0, 100 mg • L ~ l ) of PZH. MTT assay and colony formation assay were used to calculate cell viability and cell survival. Western blot was used to determine the expression of Bax, Bcl-2, cleaved caspase-3, cleaved caspase-9, and ANXA1/VEGF signaling pathway protein, such as ANXA1, VEGF, VEGFR, NF-KB P 5 0 . Results Compared with normal group, different concentrations of PZH inhibited HepG2 cells in a dose-dependent manner, inhibited the colony formation, promoted the expression of apoptotic expression, promoted the expression of ANXA1 protein, inhibited the expression of VEGF, VEGFR, and N F - K B P 5 0 as well. Conclusions PZH can inhibit the activity of HepG2 cells in vitro. Its main mechanism is related to the promotion of apoptotic protein in HepG2 cells, the promotion of cell ANXA1 protein, and the inhibition of VEGF/VEGF receptor and NF-KB signaling pathway.