Ginsenoside Rc from Panax Ginseng Ameliorates Palmitate-Induced UB/OC-2 Cochlear Cell Injury

Abstract

By 2050, at least 700 million people will require hearing therapy while 2.5 billion are projected to suffer from hearing loss. Sensorineural hearing loss (SNHL) arises from the inability of the inner ear to convert fluid waves into neural electric signals because of injury to cochlear hair cells that has resulted in their death. In addition, systemic chronic inflammation implicated in other pathologies may exacerbate cell death leading to SNHL. Phytochemicals have emerged as a possible solution because of the growing evidence of their anti-inflammatory, antioxidant, and anti-apoptotic properties. Ginseng and its bioactive molecules, ginsenosides, exhibit effects that suppress pro-inflammatory signaling and protect against apoptosis. In the current study, we investigated the effects of ginsenoside Rc (G-Rc) on UB/OC-2 primary murine sensory hair cell survival in response to palmitate-induced injury. G-Rc promoted UB/OC-2 cell survival and cell cycle progression. Additionally, G-Rc enhanced the differentiation of UB/OC-2 cells into functional sensory hair cells and alleviated palmitate-induced inflammation, endoplasmic reticulum stress, and apoptosis. The current study offers novel insights into the effects of G-Rc as a potential adjuvant for SNHL and warrants further studies elucidating the molecular mechanisms.

Unveiling the Role of Oxidative Stress in Cochlear Hair Cell Death: Prospective Phytochemical Therapeutics against Sensorineural Hearing Loss

“…Additionally, cochlear hair cell death can be induced through the activation of the unfolded protein response and ER stress. Palmitate induces apoptosis in UB/OC-2 cells through the activation of ER stress and inflammation in addition to increasing the generation of ROS [219]. The inhibition of only one of these stress pathways is insufficient to block cell death; however, ginsenoside-Rc protected against palmitate-induced cell death through the amelioration of all three pathways [219].…”

“…Palmitate induces apoptosis in UB/OC-2 cells through the activation of ER stress and inflammation in addition to increasing the generation of ROS [219]. The inhibition of only one of these stress pathways is insufficient to block cell death; however, ginsenoside-Rc protected against palmitate-induced cell death through the amelioration of all three pathways [219]. An alternative mechanism of protection also includes a reduction of PARP cleavage after gentamicin exposure in HEI-OC1 cells treated with ginsenoside-Rb1 and -Rb2 [214].…”