Cissus verticillata Extract Decreases Neuronal Damage Induced by Oxidative Stress in HT22 Cells and Ischemia in Gerbils by Reducing the Inflammation and Phosphorylation of MAPKs

Abstract

In the present study, we examined the effects of Cissus verticillata leaf extracts (CVE) against hydrogen peroxide (H2O2)- and ischemia-induced neuronal damage in HT22 cells and gerbil hippocampus. Incubation with CVE produced concentration-dependent toxicity in HT22 cells. Significant cellular toxicity was observed with >75 μg/mL CVE. CVE treatment at 50 μg/mL ameliorated H2O2-induced reactive oxygen species formation, DNA fragmentation, and cell death in HT22 cells. In addition, incubation with CVE significantly mitigated the increase in Bax and decrease in Bcl-2 induced by H2O2 treatment in HT22 cells. In an in vivo study, the administration of CVE to gerbils significantly decreased ischemia-induced motor activity 1 d after ischemia, as well as neuronal death and microglial activation 4 d after ischemia, respectively. CVE treatment reduced the release of interleukin-1β, interleukin-6, and tumor necrosis factor-α 6 h after ischemia. Furthermore, CVE treatment significantly ameliorated ischemia-induced phosphorylation of c-Jun N-terminal kinase, extracellular signal-regulated kinase 1/2, and p38. These results suggest that CVE has the potential to reduce the neuronal damage induced by oxidative and ischemic stress by reducing the inflammatory responses and phosphorylation of MAPKs, suggesting that CVE could be a functional food to prevent neuronal damage induced by ischemia.

Extracts from the Leaves of Cissus verticillata Ameliorate High-Fat Diet-Induced Memory Deficits in Mice

“…The CVE was obtained as previously described [ 52 ]. Briefly, the leaves were dried at 60 °C for 48 h and the dried leaves were homogenized for 2 min to the smallest possible particle size (approximately 200 μm) using a blender, and extracted (500 g/5 L) using the water extraction method (100 °C for 3 h) with a reflux condenser.…”

PDPOB Exerts Multiaspect Anti-Ischemic Effects Associated with the Regulation of PI3K/AKT and MAPK Signaling Pathways

“…Beginning with severe focal hypoperfusion, ischemic stroke features in the disruption of blood flow and hence neuronal damage, which proceeds upon reperfusion and evolves over time, eventually leading to rapid neuronal death. , Meanwhile, a sterile inflammatory response is triggered by the damage-associated molecular patterns (DAMPs) produced by damaged brain tissue, which leads to the well-orchestrated temporal and spatial infiltration of various immune cells. , Microglia, the immunocytes residing in the brain, are the first to respond to post-ischemic neuroinflammation accompanied by the overproduction of proinflammatory cytokines . Recently, therapeutic strategies to simultaneously combat neuronal damage and microglial inflammation have attracted great attention. − …”