Our previous studies have provided evidences that calycosin can protect the brain from ischemia/reperfusion injury, but its mechanisms is not fully understand. Transient receptor potential canonical 6 (TRPC6) has a critical role in promoting neuronal survival against cerebral ischemic injury. The aim of the present study is to test whether calycosin protects against cerebral ischemic injury through TRPC6-CREB pathway. In vivo, rats were subjected to transient middle cerebral artery occlusion (MCAO) for 2 h and then treated with different doses of calycosin at the onset of reperfusion. In vitro, primary cultured neurons were treated by calycosin, then exposed to 2 h oxygen glucose deprivation (OGD) followed by 24 h reoxygenation. Our results showed that treatment with calycosin protected against ischemia-induced damages by increasing TRPC6 and P-CREB expression and inhibiting calpain activation. The neuroprotection effect of calycosin was diminished by inhibition or knockdown of TRPC6 and CREB. These findings indicated that the potential neuroprotection mechanism of calycosin was involved with TRPC6-CREB pathway.

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Acupuncture is widely used for knee osteoarthritis (KOA) treatment in clinical practice. In the present study, we aimed to set a standard KOA animal model for electroacupuncture (EA) study and provide an acupuncture recipe for further KOA studies. Rats intra-articularly administered monosodium iodoacetate (MIA, 0.3, 1 or 3 mg respectively, n=12 each) were evaluated for pain-like behavior: paw withdrawal mechanical threshold, weight bearing deficit, and joint pathological changes (OARSI score) until 28 days after injury. Then by using the suitable dose (1 mg MIA), therapeutic effects of EA treatment (bilateral ST36 and ST35 acupoints, 2/10 Hz, 30 min/d, 6d/w, 2w) were evaluated in 3 groups (n=16 each): Early-on EA, Mid-term EA and Delayed EA, in which EA was started on day 1, day 7 or day 14 after MIA injection. Both 1 mg and 3 mg MIA induced significant joint damage and persistent pain behavior. But animals accepted 3 mg MIA rapidly developed cartilage and bone damage within 14 days. Early-on EA treatment provided significant pain relief and joint structure preservation in KOA rats. Mid-term EA treatment only reduced pain, while delayed EA treatment resulted in no effects in both aspects. 1 mg of MIA produces steady pain behavior and progressive joint damage, which was suitable for EA treatment evaluation. Early-on EA treatment provided both joint protection and pain reduction, while Mid-term EA could only be used for studying EA-induced analgesia in KOA.