Bin Na Hong

Publications of Bin Na Hong

• Curculigo orchioides, natural compounds for the treatment of noise-induced hearing loss in mice.

  Authors: Bin Na Hong, Yong-Ouk You, Tong Ho Kang

  Archives of pharmacal research. 04/2011; 34(4):653-9.

  Noise exposure is one of the most common causes of hearing loss. Noise-induced hearing loss (NIHL) is thought to primarily involve damage to the sensory hair cells of the cochlea via mechanical andNoise exposure is one of the most common causes of hearing loss. Noise-induced hearing loss (NIHL) is thought to primarily involve damage to the sensory hair cells of the cochlea via mechanical and metabolic mechanisms. Curculigo orchioides Gaerten (C. orchioides) is considered to have immunostimulant, hepatoprotective, antioxidative, anticancer, and antidiabetic activities. But the effect of C. orchioides on NIHL is not yet reported, this study focused on examining the therapeutic effects of C. orchioides on NIHL in a mouse model. Oral treatment with the extract of C. orchioides began 24 h following an examination that determined a shift in hearing threshold induced by noise exposure. Hearing threshold shifts were assessed by analyzing auditory brainstem responses at 1, 5, and 7 days following noise exposure. Central auditory function was evaluated using auditory middle latency responses, and cochlear function was determined based on transient-evoked otoacoustic emissions. C. orchioides reduced hearing threshold shifts, central auditory function damage, and cochlear function deficits. Our results suggest that C. orchioides can be utilized as a potential therapeutic natural product for NIHL.

• Diosgenin from Dioscorea nipponica ameliorates diabetic neuropathy by inducing nerve growth factor.

  Authors: Tong Ho Kang, Eunjung Moon, Bin Na Hong, Sang Zin Choi, Miwon Son, Ji-Ho Park, Sun Yeou Kim

  Biological & pharmaceutical bulletin. 01/2011; 34(9):1493-8.

  Diabetic neuropathy is characterized by axonal degeneration, demyelination, and atrophy in association with failed axonal regeneration, remyelination, and synaptogenesis. Recent reports suggest thatDiabetic neuropathy is characterized by axonal degeneration, demyelination, and atrophy in association with failed axonal regeneration, remyelination, and synaptogenesis. Recent reports suggest that reduced levels of nerve growth factor (NGF) may play a significant role in the pathogenesis of diabetic polyneuropathy. In this study, we investigated the regulation of NGF by steroid diosgenin (DG) in a diabetic neuropathy rodent model. We found that DG, the primary spirostane-type steroid in several Dioscorea species, increased NGF levels in the sciatic nerve of diabetic rats. Additionally, DG increased neurite outgrowth in PC12 cells and enhanced nerve conduction velocities in the diabetic neuropathy mouse model. DG-treated diabetic mice showed reduced disarrangement of the myelin sheath and increased area of myelinated axons by electron microscope studies and exhibited improvement in the damaged axons. Our data further suggest that DG increased the nerve conduction velocity through induction of NGF. Thus, our findings indicate that DG, a major sapogenin obtained from Dioscorea nipponica, reverses functional and ultrastructural changes and induces neural regeneration in a diabetic neuropathy model.

• Post-exposure treatment with ginsenoside compound K ameliorates auditory functional injury associated with noise-induced hearing loss in mice.

  Authors: Bin Na Hong, Se Young Kim, Tae Hoo Yi, Tong Ho Kang

  Neuroscience letters. 10/2010; 487(2):217-22.

  Noise-induced hearing loss (NIHL) is thought to primarily involve damage to the sensory hair cells of the cochlea via mechanical and metabolic mechanisms. Unfortunately, initial studies assessing theNoise-induced hearing loss (NIHL) is thought to primarily involve damage to the sensory hair cells of the cochlea via mechanical and metabolic mechanisms. Unfortunately, initial studies assessing the effectiveness of post-exposure treatment after hearing loss have yielded largely disappointing results. This study explored the effects of oral treatment with Korean red ginseng (RG) and with two bioavailable ginsenoside metabolites, ginsenoside Rh1 and ginsenoside compound K (GCK), in response to NIHL in a murine model. Pharmacological treatments began 24h after noise exposure and were continued once daily for 7 days. Central auditory function was evaluated using auditory middle latency responses, and cochlear function was determined based on transient evoked otoacoustic emissions. Additionally, cochlear hair cell morphology was investigated after noise exposure. Both Korean red ginseng and compound K reduced threshold shifts, central auditory function damage, and cochlear functional and morphological deficits. In contrast, treatment with ginsenoside Rh1 did not result in recovery of NIHL in mice. These results suggest that consumption of Korean red ginseng may facilitate recovery from noise-induced hearing loss. Furthermore, one of the active constituents in ginseng is likely ginsenoside compound K.

• Effect of baicalein from Scutellaria baicalensis on prevention of noise-induced hearing loss.

  Authors: Tong Ho Kang, Bin Na Hong, Channy Park, Se-Young Kim, Raekil Park

  Neuroscience letters. 12/2009;

  Noise-induced hearing loss (NIHL) has been thought to primarily involve damage to the sensory hair cells of the cochlea via mechanical and metabolic mechanisms. This study examined the effects ofNoise-induced hearing loss (NIHL) has been thought to primarily involve damage to the sensory hair cells of the cochlea via mechanical and metabolic mechanisms. This study examined the effects of baicalin, baicalein, and Scutellaria baicalensis (SB) extract against NIHL in a mouse model. Mice received oral treatment with SB, baicalin, baicalein beginning 30min prior to noise exposure and continuing once daily throughout the study. Hearing threshold shift was assessed by auditory brain stem responses for 35 days following noise exposure. Central auditory function was evaluated by auditory middle latency responses. Cochlear function was determined based on transient evoked otoacoustic emissions. SB significantly reduced threshold shift, central auditory function damage, and cochlear function deficits, suggesting that SB may protect auditory function in NIHL and that the active constituent may be a flavonoid, baicalein.

• High-dosage pyridoxine-induced auditory neuropathy and protection with coffee in mice.

  Authors: Bin Na Hong, Tae-Hoo Yi, Sun Yeou Kim, Tong Ho Kang

  Biological & pharmaceutical bulletin. 04/2009; 32(4):597-603.

  Auditory neuropathy (AN) is a hearing disorder characterized by an abnormal auditory brainstem response (ABR). This study examined experimental AN model induced in mice following increased dosages ofAuditory neuropathy (AN) is a hearing disorder characterized by an abnormal auditory brainstem response (ABR). This study examined experimental AN model induced in mice following increased dosages of pyridoxine. Induced AN was examined for </=10 weeks following the last pyridoxine treatment. To assess AN, we evaluated the ABR, auditory middle latency response (AMLR), otoacoustic emission (OAE), and histochemical morphology of the auditory nerve. Pyridoxine-treated mice exhibited an increase in the hearing threshold shift and delayed latency of both ABR and AMLR in proportion to pyridoxine dosage. Additionally, the extent of auditory nerve fiber loss increased in a dose-dependent manner following pyridoxine intoxication. Coffee or trigonelline treatment ameliorated the hearing threshold shift, delayed latency of the auditory evoked potential, and improved sensory fiber loss induced by pyridoxine intoxication. The present findings demonstrate that high-dose pyridoxine administration can be used to produce a new mouse model for AN, and coffee or trigonelline as a main active compound of coffee extract can potentially facilitate recovery from pyridoxine-induced auditory neuropathy.

• High dosage sildenafil induces hearing impairment in mice.

  Authors: Bin Na Hong, Tae-Hoo Yi, Sun Yeou Kim, Tong Ho Kang

  Biological & pharmaceutical bulletin. 11/2008; 31(10):1981-4.

  Sildenafil is widely administered for the treatment of erectile dysfunction. Recently, sensorineural hearing loss following the ingestion of sildenafil was reported in one male patient. We examinedSildenafil is widely administered for the treatment of erectile dysfunction. Recently, sensorineural hearing loss following the ingestion of sildenafil was reported in one male patient. We examined hearing in mice that were administered high doses of sildenafil for up to 105 d. To assess hearing impairment, we evaluated auditory brainstem responses, auditory middle latency responses, and otoacoustic emissions. At high doses, sildenafil increased the hearing threshold shift of auditory brainstem responses. High-dose sildenafil treatment also resulted in delayed latency of both auditory brainstem responses and auditory middle responses. Otoacoustic emissions differed between control and high-dose sildenafil groups with long-term treatment. Collectively, these data demonstrate that high-dose and long-term sildenafil administration can induce hearing impairment in mice.

• Coffee improves auditory neuropathy in diabetic mice.

  Authors: Bin Na Hong, Tae-Hoo Yi, Raekil Park, Sun Yeou Kim, Tong Ho Kang

  Neuroscience letters. 07/2008;

  Coffee is a widely consumed beverage and has recently received considerable attention for its possible beneficial effects. Auditory neuropathy is a hearing disorder characterized by an abnormalCoffee is a widely consumed beverage and has recently received considerable attention for its possible beneficial effects. Auditory neuropathy is a hearing disorder characterized by an abnormal auditory brainstem response. This study examined the auditory neuropathy induced by diabetes and investigated the action of coffee, trigonelline, and caffeine to determine whether they improved diabetic auditory neuropathy in mice. Auditory brainstem responses, auditory middle latency responses, and otoacoustic emissions were evaluated to assess auditory neuropathy. Coffee or trigonelline ameliorated the hearing threshold shift and delayed latency of the auditory evoked potential in diabetic neuropathy. These findings demonstrate that diabetes can produce a mouse model of auditory neuropathy and that coffee consumption potentially facilitates recovery from diabetes-induced auditory neuropathy. Furthermore, the active constituent in coffee may be trigonelline.

• Auditory neuropathy in streptozotocin-induced diabetic mouse.

  Authors: Bin Na Hong, Tong Ho Kang

  Neuroscience letters. 03/2008; 431(3):268-72.

  An investigation of the mechanism of damage to the peripheral nervous system and central nervous system in diabetes mellitus (DM) is highly important in current neurological research. AuditoryAn investigation of the mechanism of damage to the peripheral nervous system and central nervous system in diabetes mellitus (DM) is highly important in current neurological research. Auditory neuropathy is a hearing disorder in which the auditory brainstem evoked potential is absent or severely abnormal. This study investigated auditory neuropathy caused by streptozotocin in mouse model. In order to assess diabetic auditory neuropathy, we evaluated auditory brainstem response (ABR) for the evaluation of sensorineural function in peripheral auditory nerve. Auditory middle latency response (AMLR) was employed to assess the middle response in the midbrain. STZ groups significantly increased the absolute latencies IV and the interpeak latencies I-III and I-IV of ABR compared with STZ 0 group. Pa latency of AMLR also significantly increased in proportion to STZ dosage. Taken together, our results demonstrate that STZ-induced DM may impair the auditory pathway from peripheral auditory nerve to midbrain in the mouse model. We suggest that the STZ-induced diabetic mouse model may be useful for the evaluation of auditory pathway impairment by using ABR and AMLR tests.

• Coffee improves auditory neuropathy in diabetic mice

  Authors: Bin Na Hong, Tae Hoo Yi, Raekil Park, Sun Yeou Kim, Tong Ho Kang

  Neuroscience Letters.

  Coffee is a widely consumed beverage and has recently received considerable attention for its possible beneficial effects. Auditory neuropathy is a hearing disorder characterized by an abnormalCoffee is a widely consumed beverage and has recently received considerable attention for its possible beneficial effects. Auditory neuropathy is a hearing disorder characterized by an abnormal auditory brainstem response. This study examined the auditory neuropathy induced by diabetes and investigated the action of coffee, trigonelline, and caffeine to determine whether they improved diabetic auditory neuropathy in mice. Auditory brainstem responses, auditory middle latency responses, and otoacoustic emissions were evaluated to assess auditory neuropathy. Coffee or trigonelline ameliorated the hearing threshold shift and delayed latency of the auditory evoked potential in diabetic neuropathy. These findings demonstrate that diabetes can produce a mouse model of auditory neuropathy and that coffee consumption potentially facilitates recovery from diabetes-induced auditory neuropathy. Furthermore, the active constituent in coffee may be trigonelline.

• Auditory neuropathy in streptozotocin-induced diabetic mouse

  Authors: Bin Na Hong, Tong Ho Kang

  Neuroscience Letters.

  An investigation of the mechanism of damage to the peripheral nervous system and central nervous system in diabetes mellitus (DM) is highly important in current neurological research. AuditoryAn investigation of the mechanism of damage to the peripheral nervous system and central nervous system in diabetes mellitus (DM) is highly important in current neurological research. Auditory neuropathy is a hearing disorder in which the auditory brainstem evoked potential is absent or severely abnormal. This study investigated auditory neuropathy caused by streptozotocin in mouse model. In order to assess diabetic auditory neuropathy, we evaluated auditory brainstem response (ABR) for the evaluation of sensorineural function in peripheral auditory nerve. Auditory middle latency response (AMLR) was employed to assess the middle response in the midbrain. STZ groups significantly increased the absolute latencies IV and the interpeak latencies I–III and I–IV of ABR compared with STZ 0 group. Pa latency of AMLR also significantly increased in proportion to STZ dosage. Taken together, our results demonstrate that STZ-induced DM may impair the auditory pathway from peripheral auditory nerve to midbrain in the mouse model. We suggest that the STZ-induced diabetic mouse model may be useful for the evaluation of auditory pathway impairment by using ABR and AMLR tests.