1.Protective Mechanism of Electroacupuncture on Peripheral Neurotoxicity Induced by Oxaliplatin in Rats.
Feng-Jiao WANG ; She SHI ; Yong-Qiang WANG ; Ke WANG ; Shen-Dong FAN ; Ya-Nan ZHANG ; Chen-Chen FENG ; Zi-Yong JU
Chinese journal of integrative medicine 2022;28(9):833-839
OBJECTIVE:
To study the effect of electroacupuncture (EA) on oxaliplatin-induced peripheral neuropathy (OIPN) in rats.
METHODS:
Male Sprague-Dawley rats were equally divided into 3 groups using a random number table: the control group, the OIPN group, and the EA (OIPN + EA) group, with 10 rats in each. The time courses of mechanical, cold sensitivity, and microcirculation blood flow intensity were determined. The morphology of the dorsal root ganglion (DRG) was observed by electron microscopic examination. The protein levels of nuclear factor E2-related factor 2 (Nrf2), heme oxygenase-1 (HO-1), and the transient receptor potential (TRP) protein family in DRGs were assayed by Western blot.
RESULTS:
EA treatment significantly reduced mechanical allodynia and cold allodynia in OIPN rats (P<0.01). Notably, oxaliplatin treatment resulted in impaired microcirculatory blood flow and pathomorphological defects in DRGs (P<0.01). EA treatment increased the microcirculation blood flow and attenuated the pathological changes induced by oxaliplatin (P<0.01). In addition, the expression levels of Nrf2 and HO-1 were down-regulated, and the TRP protein family was over-expressed in the DRGs of OIPN rats (P<0.01). EA increased the expression levels of Nrf2 and HO-1 and decreased the level of TRP protein family in DRG (P<0.05 or P<0.01).
CONCLUSION
EA may be a potential alternative therapy for OIPN, and its mechanism may be mainly mediated by restoring the Nrf2/HO-1 signaling pathway.
Animals
;
Electroacupuncture/methods*
;
Hyperalgesia/therapy*
;
Male
;
Microcirculation
;
NF-E2-Related Factor 2
;
Oxaliplatin/adverse effects*
;
Peripheral Nervous System Diseases/chemically induced*
;
Rats
;
Rats, Sprague-Dawley
2.Incidence and Risk of Peripheral Neuropathy Caused by Intravenous and Subcutaneous Injection of Bortezomib.
Zhi-Qiang LIU ; Hai-Long XIA ; Cheng-Jun LI ; Lei XIA
Journal of Experimental Hematology 2019;27(5):1654-1663
OBJECTIVE:
To compare the effects of intravenous and subcutaneous injection of bortezomib on incidence and relative risk of peripheral neuropathy in patients with multiple myeloma(MM).
METHODS:
The electronic database of PubMed, Embase, Cochrance library, CNKI and related meeting records were searched by computers. The data were derived all from a matched randomized controlled studies. The incidence, relative risk(RR) and 95% confidence interval of peripheral neuropathy caused by intravenous and subcustaneous injections were calculated by the statistical methods.
RESULTS:
Four RCT studies were selected for meta-analysis, with a total of 911 patients (479 cases and 432 cases in the subcutaneous injection and intravenous injection groups, respectively). The incidence of peripheral neuropathy in the intravenous injection group was 41.4% (95% CI=0.137-0.692, P=0.003), and the incidence of >2 grade of peripheral neuropathy was 15.6% (95% CI=0.005-0.308, P=0.043). The corresponding incidence rates of the subcutaneous injection group were 16% (95% CI=0.021-0.299, P=0.024) and 3.4% (95% CI=-0.011-0.080, P=0.141) respectively. Compared with the intravenous injection group, the RR of peripheral neuropathy and the relative risk of peripheral neuropathy above grade 2 were 0.525, 95% CI=0.297-0.928 (P=0.027) and 0.376, 95% CI=0.196-0.722 (P=0.003) respectively.
CONCLUSION
Subcutaneous injection of bortezomib at therapeutic doses significantly reduces the incidence of peripheral neuropathy compared with intravenous injection.
Antineoplastic Agents
;
Bortezomib
;
adverse effects
;
Humans
;
Incidence
;
Injections, Subcutaneous
;
Multiple Myeloma
;
Peripheral Nervous System Diseases
;
chemically induced
3.Peripheral neuropathy induced by drinking water contaminated with low-dose arsenic in Myanmar.
Hitoshi MOCHIZUKI ; Khin Phyu PHYU ; Myo Nanda AUNG ; Phyo Wai ZIN ; Yasunori YANO ; Moe Zaw MYINT ; Win Min THIT ; Yuka YAMAMOTO ; Yoshitaka HISHIKAWA ; Kyaw Zin THANT ; Masugi MARUYAMA ; Yoshiki KURODA
Environmental Health and Preventive Medicine 2019;24(1):23-23
BACKGROUND:
More than 140 million people drink arsenic-contaminated groundwater. It is unknown how much arsenic exposure is necessary to cause neurological impairment. Here, we evaluate the relationship between neurological impairments and the arsenic concentration in drinking water (ACDW).
PARTICIPANTS AND METHODS:
A cross-sectional study design was employed. We performed medical examinations of 1867 residents in seven villages in the Thabaung township in Myanmar. Medical examinations consisted of interviews regarding subjective neurological symptoms and objective neurological examinations of sensory disturbances. For subjective neurological symptoms, we ascertained the presence or absence of defects in smell, vision, taste, and hearing; the feeling of weakness; and chronic numbness or pain. For objective sensory disturbances, we examined defects in pain sensation, vibration sensation, and two-point discrimination. We analyzed the relationship between the subjective symptoms, objective sensory disturbances, and ACDW.
RESULTS:
Residents with ACDW ≥ 10 parts per billion (ppb) had experienced a "feeling of weakness" and "chronic numbness or pain" significantly more often than those with ACDW < 10 ppb. Residents with ACDW ≥ 50 ppb had three types of sensory disturbances significantly more often than those with ACDW < 50 ppb. In children, there was no significant association between symptoms or signs and ACDW.
CONCLUSION
Subjective symptoms, probably due to peripheral neuropathy, occurred at very low ACDW (around 10 ppb). Objective peripheral nerve disturbances of both small and large fibers occurred at low ACDW (> 50 ppb). These data suggest a threshold for the occurrence of peripheral neuropathy due to arsenic exposure, and indicate that the arsenic concentration in drinking water should be less than 10 ppb to ensure human health.
Adolescent
;
Adult
;
Arsenic
;
analysis
;
toxicity
;
Cross-Sectional Studies
;
Dietary Exposure
;
adverse effects
;
Dose-Response Relationship, Drug
;
Drinking Water
;
adverse effects
;
chemistry
;
Female
;
Groundwater
;
chemistry
;
Humans
;
Male
;
Middle Aged
;
Myanmar
;
epidemiology
;
Peripheral Nervous System Diseases
;
chemically induced
;
epidemiology
;
physiopathology
;
Sensation Disorders
;
chemically induced
;
epidemiology
;
physiopathology
;
Water Pollutants, Chemical
;
analysis
;
toxicity
;
Young Adult
4.Potential application of the Kampo medicine goshajinkigan for prevention of chemotherapy-induced peripheral neuropathy.
Marco CASCELLA ; Maria Rosaria MUZIO
Journal of Integrative Medicine 2017;15(2):77-87
Chemotherapy-induced peripheral neuropathy (CIPN) is one of the most common and severe adverse effects related to cancer treatment. Unfortunately, although several agents and protocols have been proposed, no prophylactic strategies have yet to be proven useful. Therefore, new alternative therapies have been considered for CIPN prevention. Herbal medicine in Japan, called Kampo medicine, is derived from traditional Chinese medicine. Goshajinkigan (GJG) is a Kampo medicine, that is comprised of ten herbs. The aim of this work is to analyse the results of pre-clinical and clinical studies on the potential applications of GJG in CIPN prevention.
Antineoplastic Agents
;
adverse effects
;
Drugs, Chinese Herbal
;
therapeutic use
;
Humans
;
Medicine, Kampo
;
Peripheral Nervous System Diseases
;
chemically induced
;
prevention & control
;
Phytotherapy
5.Effect of Tanshinone IIA in Preventing and Treating Oxaliplatin Induced Peripheral Neuropathy.
Kai XU ; Wei-ting CHENG ; Zuo-wei HU ; Wang SHAN
Chinese Journal of Integrated Traditional and Western Medicine 2016;36(5):559-563
OBJECTIVETo observe preventive and therapeutic effects of Tanshinone IIA (T II A) on oxaliplatin induced peripheral neuropathy (OlPN) and to explore its effects on the expression of calcitonin gene related peptide (CGRP) and never growth factor (NGF).
METHODSTotally 36 phase II - III patients with malignant tumor of digestive tract undergoing chemotherapy program with oxaliplatin, were equally assigned to the T II A group (using THA at 80 mg/day 1 day before oxaliplatin chemotherapy for 3 successive days) and the control group (using chemotherapy program with oxaliplatin alone) by segmented randomization. After 4 cycles of chemotherapy, the incidence degree and incidence of OlPN were evaluated. Sensory nerve conduction velocity (SNCV) and motor nerve conduction velocity ( MNCV) were tested by EMG evoked potential device. Serum levels of CGRP and NGF were also detected in the two groups before and after chemotherapy. The correlation of serum levels of CGRP and NGF to OIPN was assessed using linear correlation analysis.
RESULTSAfter chemotherapy the OlPN incidence was 27.8% (5/18 cases) in the T II A group, obviously lower than that in the control group (55.6%, 10/18 cases; P < 0.05). Compared with before treatment in the same group, SNCV and MNCV of common peroneal nerve were slowed down, serum NGF levels decreased, and serum CGRP levels obviously increased in the two groups (all P < 0.05). Compared with the control group after treatment, SNCV and MNCV of common peroneal nerve were obviously accelerated, serum NGF levels increased, and serum CGRP levels obviously decreased in the THA group (all P < 0.05). Results of linear correlation analysis indicated serum NGF level was negatively correlated with peripheral neuropathy (PN), serum CGRP expression was positively correlated with neurotoxicity (P < 0.05).
CONCLUSIONT II A could reduce the incidence of OlPN, which might be associated with inhibiting the expression of CGRP and up-regulating NGF activities.
Calcitonin Gene-Related Peptide ; blood ; Diterpenes, Abietane ; therapeutic use ; Gastrointestinal Neoplasms ; drug therapy ; Humans ; Nerve Growth Factor ; blood ; Neural Conduction ; drug effects ; Organoplatinum Compounds ; adverse effects ; Peripheral Nervous System Diseases ; chemically induced ; drug therapy ; Up-Regulation
7.The Role of NF mRNA and Calpain in NF Reduction of Acrylamide Neuropathy.
Su Fang YU ; Xiao Min WEI ; Feng Feng YAN ; Shu E WANG ; Cui Li ZHANG ; Xi Wei YANG
Biomedical and Environmental Sciences 2015;28(6):445-448
The purpose of this study was to study the role of neurofilament (NF) mRNA and calpain in NF reduction of acrylamide (ACR) neuropathy. Male Wistar adult rats were injected i.p. every other day with ACR (20 mg/kg·bW or 40 mg/kg·bW) for 8 weeks. NF mRNA expression was detected using RT-PCR and the calpain concentration was determined using western blot analysis. The NF mRNA expression significantly decreased while the level of m-calpain and μ-calpain significantly increased in two ACR-treated rats groups regardless of the ACR dose. The light NF (NF-L) protein expression was significantly correlated with NF-L mRNA expression. Combined with previous data, the concentrations of three NF subunits were negatively correlated with the calpain levels. These findings suggest that NF-L mRNA and calpain mediated the reduction in NF of ACR neuropathy.
Acrylamide
;
toxicity
;
Animals
;
Calpain
;
metabolism
;
Gene Expression Regulation
;
drug effects
;
Intermediate Filaments
;
genetics
;
Male
;
Peripheral Nervous System Diseases
;
chemically induced
;
genetics
;
metabolism
;
RNA, Messenger
;
genetics
;
metabolism
;
Rats
9.Misdiagnosis of occupational chronic n-hexane poisoning: an analysis of 16 cases.
Jianjie ZHANG ; Zhiming LI ; Jinlin WANG ; Hui LI ; Tujie SI ; Lihua DENG ; Shaohong QIU
Chinese Journal of Industrial Hygiene and Occupational Diseases 2014;32(12):930-931
OBJECTIVETo analyze the cause of misdiagnosis of occupational chronic n-hexane poisoning and to investigate the diagnosis and differential diagnosis of this disease.
METHODSThe clinical data of 16 patients with occupational chronic n-hexane poisoning who had been misdiagnosed with other diseases were collected. The hospital they first visited, cause of misdiagnosis, clinical features, and the misdiagnosis rate among inpatients during the same period were retrospectively analyzed.
RESULTSSixteen of 62 patients hospitalized during the same period were misdiagnosed at the first visit; 11 cases were in the upper first-class hospitals, and 5 cases in the upper second-class hospitals; 5 cases were misdiagnosed as Green Barry syndrome, 2 cases as motor neuron disease, 2 cases as drug-induced peripheral neuropathy, 3 cases as periodic paralysis, and 4 cases had uncertain diagnosis.
CONCLUSIONMost doctors who work in ordinary hospitals do not know occupational chronic n-hexane poisoning, which is often misdiagnosed as general neuropathies or difficult diseases. The key to correct diagnosis is to know the patient's occupational history and clinical features.
Chronic Disease ; Diagnosis, Differential ; Diagnostic Errors ; Hexanes ; poisoning ; Hospitals ; Humans ; Peripheral Nervous System Diseases ; chemically induced ; Retrospective Studies
10.Changes in expression of motor protein for axonal transport in nerve tissues of carbon disulfide-intoxicated rats.
Shasha WANG ; Yuan GAO ; Yiping WANG ; Ruirui KOU ; Chaoshuang ZOU ; Keqin XIE ; Fuyong SONG
Chinese Journal of Industrial Hygiene and Occupational Diseases 2014;32(9):660-663
OBJECTIVETo study the changes in microtubule motor protein expression in the spinal cord and sciatic nerve of rats exposed to carbon disulfide, and to investigate the possible molecular mechanism of changes in axonal transport in carbon disulfide-induced peripheral neuropathy.
METHODSHealthy adult male Wistar rats were randomly divided into one control group and three experimental groups (10 rats per group). The rats in experimental groups were intoxicated by gavage of carbon disulfide at a dose of 200, 400, or 600 mg/kg 6 times a week for 6 consecutive weeks, while the rats in control group were given the same volume of corn oil by gavage. Animals were sacrificed after exposure, with nerve tissue separated. The levels of dynein, dynactin, and kinesin in the spinal cord and sciatic nerve were determined by Western blot.
RESULTSThe content of dynein, dynactin, and kinesin in the sciatic nerve decreased significantly under exposure to carbon disulfide. The levels of dynein in the sciatic nerve were reduced by 23.47% and 33.34% at exposure doses of 400 and 600 mg/kg, respectively. The levels of dynactin in the sciatic nerve of the three experimental groups were reduced by 19.91%, 24.23%, and 41.30%, respectively. The level of kinesin was reduced by 25.98%under exposure to 600 mg/kg carbon disulfide. All the differences were statistically significant (P < 0.01). As compared with the control group, the 600 mg/kg group experienced a 28.24% decrease in level of dynactin in the spinal cord (P < 0.01), but no significant change was observed in the level of dynein or kinesin.
CONCLUSIONCarbon disulfide has an impact on microtubule motor protein expression in nerve tissues, which might be involved in the development of carbon disulfide-induced peripheral neuropathy.
Animals ; Axonal Transport ; drug effects ; physiology ; Carbon Disulfide ; toxicity ; Dynactin Complex ; Male ; Microtubule-Associated Proteins ; metabolism ; Nerve Tissue ; metabolism ; Peripheral Nervous System Diseases ; chemically induced ; metabolism ; Rats, Wistar ; Sciatic Nerve ; metabolism ; Spinal Cord ; metabolism

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