Anti-VPA polyclonal antibody

Treatment of vestibular migraine currently lacks a firm scientific basis, as high quality randomized controlled trials are not available. Therefore, recommendations are largely borrowed from the migraine sphere. The first therapeutic step is explanation and reassurance. Many patients do not need pharmacological treatment, as attacks may be infrequent and tolerable. Acute attacks can be ameliorated in some patients with antiemetic drugs such as diphenhydramine, meclizine, and metoclopramide. Frequent attacks may warrant pharmacological prophylaxis with metoprolol, amitriptyline, topiramate, valproic acid, or flunarizine. Nonpharmacological measures including regular exercise, relaxation techniques, stress management, and biofeedback may be similarly effective and can be combined with a pharmacological approach. Limited data indicate that the prognosis appears to be less favorable for vestibular migraine than for migraine headaches.

Arsenic trioxide (ATO; As2O3) has anti-cancer effects in various solid tumors as well as hematological malignancy. Valproic acid (VPA), which is known to be a histone deacetylase inhibitor, has also anti-cancer properties in several cancer cells including lung cancer cells. Combined treatment of ATO and VPA (ATO/VPA) could synergistically enhance anti-cancer effects and reduce ATO toxicity ATO. In this study, the combined anti-cancer effects of ATO and VPA (ATO/VPA) was investigated in NCI-H460 and NCI-H1299 lung cancer cells in vitro and in vivo. A combination of 3 mu M ATO and 3 mM VPA (ATO/VPA) strongly inhibited the growths of both lung cancer cell types. DNA flow cytometry indicated that ATO/VPA significantly induced G2/M-phase arrest in both cell lines. In addition, ATO/VPA strongly increased the percentages of sub-G1 cells and annexin V-FITC positive cells in both cells. However, lactate dehydrogenase (LDH) release from cells was not increased in ATO/VPA-treated cells. In addition, ATO/VPA increased apoptosis in both cell types, accompanied by loss of mitochondrial membrane potential (MMP, Psi m), activation of caspases, and cleavage of anti-poly ADP ribose polymerase-1. Moreover, a pan-caspase inhibitor, Z-VAD, significantly reduced apoptotic cell death induced by ATO/VPA. In the xenograft model, ATO/VPA synergistically inhibited growth of NCI-H460-derived xenograft tumors. In conclusion, the combination of ATO/VPA effectively inhibited the growth of lung cancer cells through G2/M-phase arrest and apoptotic cell death, and had a synergistic antitumor effect in vivo.