Animal models are pivotal for understanding the mechanism of neuropathic pain and development of effective therapy for its optimal management. A battery of neuropathic pain models has been developed to simulate the clinical pain conditions with diverse etiology. The present review exhaustively discusses the methodology, behavioral alterations, limitations, and advantages of about 40 different animal models of neuropathic pain along with their modifications. Development of these models has contributed immensely in understanding the chronic pain and underlying peripheral as well as central pathogenic mechanisms. Furthermore, research has resulted in the development of new therapeutic agents for neuropathic pain management, and the preclinical data obtained using these animal models have been successively translated to effective pain management in clinical setup also. As each animal model has been created with specific methodology and results tend to vary largely with the slight changes related to methodology, therefore, it is essential that data from different models should be reported and interpreted in the context of the specific pain model.

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The present study was designed to investigate the effect of ferulic acid (FA) in vincristine-induced neuropathic pain in rats. Vincristine (50 µg/kg, i.p. for 10 consecutive days) was administered to induce painful neuropathy in rats. Various pain sensitive tests, viz., pinprick, hot plate, paint-brush, and acetone test were performed on different days (1, 6, 14, and 21) to assess the degree of mechanical hyperalgesia, heat hyperalgesia, mechanical dynamic allodynia, and cold allodynia, respectively. The electrophysiological and histopathological evaluations were also investigated. The tissue thiobarbituric acid reactive species (TBARS), reduced glutathione (GSH), myeloperoxidase (MPO), tumor necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6), interleukin-10 (IL-10), and total calcium were measured as the markers of inflammation and oxidative stress. FA (50 and 100 mg/kg, i.p.) and gabapentin (10 mg/kg, p.o.) were administered for 11 days. Administration of FA attenuated the vincristine-induced behavioral alteration along with electrophysiological and histopathological changes significantly (P < 0.05). FA also attenuated the vincristine-induced oxidative stress (TBARS, GSH, and total calcium levels) and inflammation (MPO, TNF-alpha, IL-6, and IL-10). It may be concluded that FA has ameliorative potential in mitigation of the painful states associated with vincristine-induced painful neuropathy that may further be attributed to anti-inflammatory actions with subsequent reduction in oxidative stress.

Transfersomes are particularly optimized, ultradeformable (ultraflexible) lipid supramolecular aggregates, which are able to penetrate the mammalian skin intact. Transfersome is a type of carrier system which is capable of transdermal delivery of low as well as high molecular weight drugs. Transfersomes penetrate through the pores of stratum corneum which are smaller than its size and get into the underlying viable skin in intact form. Acne vulgaris is a disease of the pilosebaceous follicle characterized by non-inflammatory (open and closed comedones) and inflammatory lesions (papules, pustules, and nodules). In such situation transdermal drug delivery remains the most preferential mode of administration. But, stratum corneum forms the most formidable barrier for the penetration of drug through skin. To overcome the stratum corneum barrier, the use of lipid vesicles like transfersomes in delivery systems has involved increasing attention in recent years. The aim of the present study was to statistically optimize the vesicular formulations (Transfersomes) for enhanced skin delivery of a model drug Clindamycin Phosphate. Keywords: Transfersomes, Acne vulgaris, Clindamycin Phosphate

BackgroundInjury to a nerve is the most common reason of acquired peripheral neuropathy. Therefore, searching for effective substance to recover of nerve after injury is need of present era. The current study investigates the protective potential of Standardized Fruit Extract of Punica granatum L (PFE) [Ellagic acid (41.6%), Punicalagins (10%), Granatin (5.1%)] in Tibial & Sural Nerve Transection (TST) induced neuropathic pain in rats.MethodsTST was performed by sectioning tibial and sural nerve portions of the sciatic nerve and leaving the common peroneal nerve intact. Acetone drop, pin-prick, hot plate, paint brush & Walking Track tests were performed to assess cold allodynia; mechanical heat, hyperalgesia and dynamic mechanical allodynia & tibial functional index respectively. The levels of TNF-α, TBARS, GSH and Nitrite were measured in the sciatic nerve as an index of inflammation & oxidative stress.ResultsTST led to significant development of cold allodynia; mechanical and heat hyperalgesia; dynamic mechanical allodynia; functional deficit in walking along with rise in the levels of TBARS, TNF-α, GSH and Nitrite. Administrations of PFE (100 & 300 mg/kg oral), significantly attenuate TST induced behavioral & biochemical changes. Pretreatments of BADGE (120 mg/kg IP) a PPAR-γ antagonist and nitric oxide precursor L-arginine (100 mg/kg IP) abolished the protective effect of PFE. Whereas, pretreatment of L-NAME (5 mg/kg IP) a NOS inhibitor significantly potentiated PFE’s protective effect of PFE.ConclusionPFE shown to have attenuating effect in TST induced neuropathic pain which may be attributed to potential PPAR-gamma agonistic activity, nitric oxide inhibitory, anti-inflammatory and anti oxidative actions.