Liu Jun Zi Tang-A Potential, Multi-Herbal Complementary Therapy for Chemotherapy-Induced Neurotoxicity

• Published in: International journal of molecular sciences Vol. 19; no. 4; p. 1258
• Main Authors: Chiou, Chun-Tang, Wang, Kaw-Chen, Yang, Ying-Chen, Huang, Chuen-Lin, Yang, Sien-Hung, Kuo, Yao-Haur, Huang, Nai-Kuei
• Format: Journal Article
• Language: English
• Published: Switzerland MDPI AG 23.04.2018; MDPI
• Subjects: Animals; Apoptosis; Apoptosis - drug effects; Attenuation; Cancer therapies; Cell Line, Tumor; Chemotherapy; Chinese medicine; Cisplatin; Cisplatin - toxicity; Cytotoxicity; Deoxyribonucleic acid; DNA; Drug dosages; Drugs, Chinese Herbal - therapeutic use; Dyspepsia; Free radicals; Functionals; Gene expression; Herbal medicine; Humans; Hyperalgesia; Hyperalgesia - chemically induced; Hyperalgesia - drug therapy; Kinases; Liu Jun Zi Tang; Membrane potential; Membrane Potential, Mitochondrial - drug effects; Mice; Mitochondria; Mitochondrial DNA; Neurotoxicity; Neurotoxicity Syndromes; Pain; Pain perception; Peripheral neuropathy; Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha - metabolism; PGC-1α; Physiology; Quality of life; Taiwan; Liu Jun Zi Tang; PGC-1α; neurotoxicity; cisplatin; mitochondria
• ISSN: 1422-0067; 1661-6596; 1422-0067
• DOI: 10.3390/ijms19041258

Liu Jun Zi Tang (LJZT) has been used to treat functional dyspepsia and depression, suggesting its effects on gastrointestinal and neurological functions. LJZT is currently used as a complementary therapy to attenuate cisplatin-induced side effects, such as dyspepsia. However, its effect on chemotherapy-induced neuropathic pain or neurotoxicity has rarely been studied. Thus, we explored potential mechanisms underlying LJZT protection against cisplatin-induced neurotoxicity. We observed that LJZT attenuated cisplatin-induced thermal hyperalgesia in mice and apoptosis in human neuroblastoma SH-SY5Y cells. Furthermore, it also attenuated cisplatin-induced cytosolic and mitochondrial free radical formation, reversed the cisplatin-induced decrease in mitochondrial membrane potential, and increased the release of mitochondrial pro-apoptotic factors. LJZT not only activated the peroxisome proliferator-activated receptor gamma coactivator 1-alpha ( ) promoter region, but also attenuated the cisplatin-induced reduction of expression. Silencing of the gene counteracted the protection of LJZT. Taken together, LJZT mediated, through anti-oxidative effect and mitochondrial function regulation, to prevent cisplatin-induced neurotoxicity.