LRP2 in SHH-dependent adult neurogenesis

Bunatyan, Lena; Christ, Annabel; Gajera, Chandresh R.; Hammes-Lewin, Annette; Willnow, Thomas E.

doi:10.1016/j.mod.2017.04.313

Cited by 1 publication

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“…In addition, Bunatyan et al suggested that the loss of ependymal LRP2 in mice resulted in a significant decrease in the proliferation of SVZ. Consistent with neurological damage in SVZ, the number of newly generated neurons reaching the olfactory bulb was significantly reduced, indicating the role of LRP2 in controlling adult neurogenesis in SVZ, which may involve balancing the morphogenetic signals provided by SHH and BMP4 33…”

Section: Discussionmentioning

confidence: 83%

<p>Rutaecarpine may improve neuronal injury, inhibits apoptosis, inflammation and oxidative stress by regulating the expression of ERK1/2 and Nrf2/HO-1 pathway in rats with cerebral ischemia-reperfusion injury</p>

Han¹,

Hu²,

Chen³

2019

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BackgroundCerebral ischemia-reperfusion (CI/R) injury is a more serious brain injury caused by the recovery of blood supply after cerebral ischemia for a certain period of time. Rutaecarpine (Rut) is an alkaloid isolated from Evodia officinalis with various biological activities. Previous studies have shown that Rut has a certain protective effect on ischemic brain injury, but the specific molecular mechanism is still unknown.MethodsIn this study, a rat model of CI/R was established to explore the effects and potential molecular mechanisms of Rut on CI/R injury in rats.ResultsThe results showed that Rut alleviated neuronal injury induced by CI/R in a dose-dependent manner. Besides, Rut inhibited neuronal apoptosis by inhibiting the activation of caspase 3 and the expression of Bax. In addition, Rut alleviated the inflammatory response and oxidative stress caused by CI/R through inhibiting the production of pro-inflammatory factors (IL-6 and IL-1β), lactate dehydrogenase (LDH), malondialdehyde (MDA) and ROS, and increased the levels of anti-inflammatory factors (IL-4 and IL-10) and superoxide dismutase (SOD). Biochemically, Western blot analyses showed that Rut inhibited the phosphorylation of ERK1/2 and promoted the expression of nuclear factor-erythroid 2 related factor 2 (Nrf2) pathway-related proteins (Nrf2, heme oxygenase 1 (HO-1) and NAD (P) H-quinone oxidoreductase 1) in a dose-dependent manner. These results show that Rut may alleviate brain injury induced by CI/R by regulating the expression of ERK1/2 and the activation of Nrf2/HO-1 pathway.ConclusionIn conclusion, these results suggest that Rut may be used as an effective therapeutic agent for damage caused by CI/R.

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Section: Discussionmentioning

confidence: 83%