Paeoniflorin protects spiral ganglion neurons from cisplatin‐induced ototoxicity: Possible relation to PINK1/BAD pathway

Abstract

The objective of this study was to elucidate whether paeoniflorin (PF) exerted an effect on cisplatin‐induced spiral ganglion neuron (SGN) damage, with special attention given to the role of PINK1/BAD pathway in this process. Middle cochlear turn culture and C57BL/6 mice were utilized to identify the character of PF in vitro and in vivo. We found that cisplatin treatment led to SGN damage, in which reactive oxygen species (ROS) generation increased, PINK1 expression decreased, BAD accumulation on mitochondria raised and mitochondrial apoptotic pathway activated. Conversely, we demonstrated that PF pre‐treatment obviously mitigated cisplatin‐induced SGN damage. Mechanistic studies showed that PF could reduce ROS levels, increase PINK1 expression, decrease the BAD accumulation on mitochondria and, thus, alleviate the activated mitochondrial apoptosis in SGNs caused by cisplatin. Overall, the findings from this work reveal the important role of PF and provide another strategy against cisplatin‐induced ototoxicity.

BRAF inhibition protects against hearing loss in mice

“…4F). Previous reports have documented cisplatin-induced damage to the stria and spiral ganglion neurons, reinforcing these cells as sensitive to cisplatin treatment (63)(64)(65)(66).…”

Recent advances in the treatment and prevention of peripheral neuropathy after multiple myeloma treatment

“…Paeoniflorin is a bioactive compound isolated from the Chinese herbal medicine plant Paeonia lactiflora , which has a wide range of anti‐inflammatory, analgesic and immunomodulatory effects 50 . In addition, paeoniflorin is a potential neuroprotective agent, which has been proved to reduce neuronal damage by reducing the secretion of IL‐6 and other inflammatory factors or reducing the level of autophagy 51–53 . Recent studies have confirmed that paeoniflorin significantly improves BIPN, which may regulate PARKIN‐mediated mitochondrial autophagy and mitochondrial damage by reducing IL‐6 levels 44 .…”

Mitochondrial Dysfunction and Therapeutic Targets in Auditory Neuropathy

“…A calpain inhibitor PD150606 could suppress calpain by mediating AIF induced by glutamine and caspase-12 activation, restraining apoptosis processing and SGNs in vitro [87]. Meanwhile, allicin [104] and curcumin [105] were found to protect SGNs from ototoxic drugs, when paeoniflorin and neurotrophin might exert as protective effect through the PINK1/BAD pathway [89,106].…”