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Discover Supplement-Drug Interactions
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Last Updated: 3 years ago
supplement:
Acetylcysteine
supplement:
Capsaicin
Research Papers that Mention the Interaction
“Moreover, NAC abrogated the effects of capsaicin on Stat3-dependent autophagy.”
Inhibiting ROS-STAT3-dependent autophagy enhanced capsaicin–induced apoptosis in human hepatocellular carcinoma cells“Co-treatment of cells with NAC and capsaicin abrogated the effects of capsaicin on autophagy and cell death.”
“Furthermore, we found that capsaicin triggered ROS generation in cells, while the levels of ROS decreased with N-acetyl-cysteine ( NAC ), a ROS scavenger.”
“The antioxidant N-acetyl-l-cysteine (NAC) acts synergistically with CAP to reduce ROS generation, without affecting CAP-induced toxicity.”
“The CAP and H2O2-induced TRPM2 current densities were also decreased by the NADPH oxidase inhibitors apocynin and N-Acetylcysteine.”
Activation of TRPM2 and TRPV1 Channels in Dorsal Root Ganglion by NADPH Oxidase and Protein Kinase C Molecular Pathways: a Patch Clamp Study“ NAC (1 g/kg/d × 7 days) prevented B1R up-regulation, superoxide anion production and NF-kB activation induced by capsaicin (15 mg/kg).”
“Our findings confirm a role for the spinal cord in NAC actions because systemic NAC administration also reduced the nociception trigged by intrathecal injection of capsaicin.”
“Systemic or spinal, but not peripheral, administration of the exogenous thiolic compound N-acetyl-L-cysteine (NAC) reduced nociception induced by intraplantar capsaicin injection.”
“In addition, NAC completely blocked phosphorylation of JNK and p38 MAPK induced by capsaicin.”
Induction of apoptosis by capsaicin in hepatocellular cancer cell line SMMC-7721 is mediated through ROS generation and activation of JNK and p38 MAPK pathways.
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