Ganglioside-monosialic acid (GM1) prevents oxaliplatin-induced peripheral neurotoxicity in patients with gastrointestinal tumors

نویسندگان

  • Yanyun Zhu
  • Junlan Yang
  • Shunchang Jiao
  • Tiefeng Ji
چکیده

BACKGROUND Oxaliplatin, an effective antineoplastic agent againstgastrointestinal tumors, can cause severe peripheral neurotoxicity, which seriously limits its clinical application. To date, there are no effective treatments for this complication. Ganglioside-monosialic acid (GM1) has been shown to protect neurons against injuries and degeneration. The aim of this study was to evaluate the effects of GM1 on preventing oxaliplatin-induced neurotoxicity in patients with gastrointestinal tumors. METHODS In this study, 120 patients with gastrointestinal tumors were enrolled, andthey received the treatment of XELOX (oxaliplatin and capecitabine) and FOLFOX4 (oxaliplatin, leukovolin and 5-fluorouracil). The patients were randomly divided into two groups, the experimental group and control group, with60 patients ineach. On the day chemotherapy was initiated, the experimental group received GM1 intravenously (100 mg once daily) for 3 days, while no neuroprotective agents were applied in the control group. The incidence rates and classification of neurotoxicity in the two groups were evaluated and the differences between the two groups were examined. Furthermore, whether GM1 affected the therapeutic effects of chemotherapy was also examined. RESULTS The grade of neurotoxicity in the experimental group was significantly lower than in the control group (P<0.05, Mann-Whitney U test). The probability of occurrence of low-grade neurotoxicity (grade 0 and 1) in the experimental group was higher than that in the control group (logistic ordinal regression); whereas the probability of occurrence of high-grade neurotoxicity (grade 2 and 3) in the experimental group was lower than in the control group (logistic ordinal regression). CONCLUSION The data suggested that GM1 could reduce the grade of oxaliplatin-induced neurotoxicity and was an effective neuroprotective agent against oxaliplatin-induced high-grade neurotoxicity in patients with gastrointestinal tumors.

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

منابع مشابه

[Prophylactic effect of amifostine on oxaliplatin-related neurotoxicity in patients with digestive tract tumors].

BACKGROUND & OBJECTIVE Oxaliplatin, an active agent used widely in treating digestive tract tumors, displays a frequent dose-limiting neurotoxicity. This study was to assess the clinical efficacy of amifostine in preventing neurotoxicity induced by oxaliplatin. METHODS A total of 92 patients with colorectal cancer or gastric cancer were enrolled, and randomly assigned to receive amifostine (5...

متن کامل

Propofol and thiopental suppress amyloid fibril formation and GM1 ganglioside expression through the γ-aminobutyric acid A receptor.

BACKGROUND The incidence of Alzheimer disease may increase after surgical interventions. Amyloid β-protein (Aβ) fibrillogenesis, which is closely related to Alzheimer disease, is reportedly accelerated by exposure to anesthetics. However, the effects of GM1 ganglioside (GM1) on Αβ fibrillogenesis have not yet been reported. The current study was designed to examine whether the anesthetics propo...

متن کامل

Oral Calcium Ameliorating Oxaliplatin-Induced Peripheral Neuropathy.

Oxaliplatin has become an integral part of the standard treatment for advanced colorectal cancer. While oxaliplatin has only mild hematologic and gastrointestinal side effects, its dose-limiting toxicity is a cumulative sensory neurotoxicity. Oxaliplatin causes a unique, but frequent, acute sensory neuropathy that is triggered or aggravated by exposure to cold but is rapidly reversible, without...

متن کامل

Gangliosides rescue neuronal cells from death after trophic factor deprivation.

Serum-free cultures of PC 12 cells have been used as a model system for studying neuronal death occurring after neurotrophic factor deprivation. In this system, NGF rescues cells from death and prevents apoptotic DNA fragmentation. We report here that GM1 also promotes long-term survival of naive and NGF-pretreated PC 12 cells in serum-free medium and prevents internucleosomal cleavage of PC 12...

متن کامل

GM1 and Tumor Necrosis Factor-A, Overexpressed in Renal Cell Carcinoma, Synergize to Induce T-Cell Apoptosis

The ability to induce T-cell apoptosis is one mechanism by which tumors evade the immune system, although the molecules involved remain controversial. We found that renal cell carcinoma (RCC)–induced T-cell apoptosis was inhibited by >50% when cocultures were performed with gangliosidedepleted tumor cells, caspase-8–negative lymphocytes, or anti–tumor necrosis factor-A (TNFA) antibodies, sugges...

متن کامل

ذخیره در منابع من


  با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

عنوان ژورنال:

دوره 11  شماره 

صفحات  -

تاریخ انتشار 2013