Studies On The Neuroprotective Effect And Mechanism Of Salidroside, DL0108 And AV

Neurodegenerative disorders are among the most puzzling and devastating illnesses in medicine. The resemblance of these diseases is that some of affected nerve cells die. After concept of neuroprotection was brought forward, treatment of neurodegenerative by neroprotective drugs became a new subject .In the present study, we investigated the neuroprotective effect and the possible mechanism. I The neuroprotective effect and mechanism of SalidrosideSalidroside (Sald), was extracted from Rhodiola rosea L, a Traditional Chinese medicine has been used for long time for anti-aging, anti-cancer and anti-oxidative stress etc. In present experiment, salidroside could protect the PC12 cell against the injuries caused by exposuring of PC12 cells to 2 mM glutamate for 15min followed by incubation with serum-free medium for 24h, which resembled the excitotoxin in vivo system. Furthermore, the saldroside could decrease the [Ca²⁺]i of PC12 cells in Mg²⁺-free Hanks' solution and D-Hanks' solution but there was no effect on basal [Ca²⁺]i in Hanks' solution. The studies also indicated that Salidroside can inhibit the increases of [Ca²⁺]i induced by KC1 and glutamate. In conclusion, salidroside may protect PC12 cell against glutamate excitotoxic damage through suppressing the excessive entry of Ca²⁺ and the release of the calcium stores.We investigated the effect of salidroside on mitochondria injury induced by sodium azide. Human neuroblastoma SH-SY5Y cells were exposed to sodium azide with different concentration of salidroside, then cell viability was measured by thiazolyl blue (MTT) method and mitochondria membrane potential (MMP) was detected by JC-1 method. Protective effect of Salidroside against disfunction of mitochondria induced by NaN₃ was detected by resazurin method. After exposing to 64 mmol/L sodium azide for 4 hours, cell viability and MMP of SH-SY5Y cells significantly decreased. When pretreated with salidroside, the cell damage was greatly decreased and the mitochondria membrane potential was maintained. Furthermore, salidroside can protect function of rat brain mitochondrial against damage induced by sodium azide.