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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 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 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 investigate the neuroprotective effect of salidroside on CoCl2 -induced hypoxia injury in PC 12 cells, and further explore the mechanism of salidroside on inhibiting complement and neuroprotection. Methods: The model of CoCl2-induced hypoxia injury in PC 12 cells was established. The expressions of Egrl, Egr4, C3 and the activity of caspase-3 were assessed with different concentrations of salidroside treatment. The expressions of Egrl, Egr4 and the activity of caspase-3 were tested with C3ar inhibitor and salidroside treatment. The expressions of Bax, Bcl-xl, C3 and the activity of caspase-3 were determined with Egr4 siRNA and salidroside treatment. Results: Salidroside significantly reduced the caspase-3 activity and the protein expression of Bax and C3, and improved the expression of Bcl-xl, Egrl, and Egr4 proteins in CoCl2-induced PC12 cells. Salidroside reduced the caspase-3 activity and the expression of Egrl, Egr4 with C3ar inhibitor treatment. With siRNA interference with the expression of Egr4, salidroside reversed the activity of caspase-3, Bax and Bcl-xl, but the effect on C3 was not obvious. Conclusions: Salidroside has neuroprotective effect on the model of CoCl2 -induced hypoxia injury in PC12 cells, which is related to the inhibition of complement component C3 and the improvement of the expression of Egr4 by salidroside.
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Aim To investigate the anti-inflammatory effect of salidroside on lipopolysaccharide (LPS)-induced BV2 microglia and its mechanism. Methods The model of LPS-induced injury in BV2 microglia was established. The expression of cytokines IL-6, IL-1β and TNF-α mRNA was detected by qPCR, and the expression of Akt, p-Akt, nuclear protein NF-κB p50 protein was dectected by Western blot with different concentrations of salidroside treatment. The model was sequentially treated with PI3K inhibitor LY294002 for 30 min, and after the treatment of salidroside, the expressions of Akt, p-Akt, nuclear protein NF-κB p50, IL-6, IL-1β, TNF-α and other indicators were dectected by Western blot. Results Compared with model, salidroside reduced the expression of IL-6, IL-1β and TNF-α mRNA in BV2 microglia, improved the expression of p-Akt protein, and reduced the nuclear protein NF-κB p50. After the treatment of LY294002, salidroside had no obvious effect on the expression of p-Akt, nuclear protein NF-κB p50, IL-6, IL-1β. Conclusions Salidroside can inhibit LPS-induced BV2 microglia inflammatory reaction by activating PI3K/Akt signaling pathway, promoting Akt phosphorylation, inhibiting NF-κB p50 nuclear transcription, and inhibiting cytokines.