Tetrahydrocurcumin exerts protective effect on vincristine induced neuropathy: Behavioral, biochemical, neurophysiological and histological evidence.

Hyperalgesia, allodynia, delayed motor nerve conduction velocity, oxidative stress and axonal damage are signs and symptoms of chemotherapy induced peripheral neuropathy (CIPN). Present treatment/preventive strategies of CIPN are futile and the neuropathy may even lead to discontinuation of chemotherapy. In this study, we evaluated the protective effect of tetrahydrocurcumin (THC) 40 and 80mg/kg in experimental vincristine induced neuropathy in rats. Hyperalgesia was assessed by hot plate (thermal), Randall-Selitto (mechanical) test, allodynia was assessed by cold plate (thermal) test, functional loss was measured by sciatic function index, nociception was evaluated by formalin test. Neurophysiological recordings were carried out to assess motor nerve conduction velocity. Total calcium levels, oxidative stress and TNF-α was measured in sciatic nerve tissue homogenate to assess neuropathy. Histopathological changes was observed on sciatic nerve to assess the protective effect of THC against the vincristine. Pregabalin was used as a standard in this study. Rats administered with THC at 80mg/kg significantly attenuated the vincristine induced neuropathic pain manifestations which may be due to its multiple actions including anti-nociceptive, anti-inflammatory, neuroprotective, calcium inhibitory and antioxidant effect. This study delineates that THC can be a promising candidate for the prevention of CIPN by chemotherapeutic agents.

Evaluation of the protective effect of Pterocarpus marsupium on acetic acid-induced ulcerative colitis in rats.

The aim of the study was to evaluate the effect of Pterocarpus marsupium (PM) on acetic acid (AA)-induced ulcerative colitis (UC) in rats. The rats were divided into five groups, each having six rats. PM extract 100 mg and 200 mg/kg was given orally to groups four and five, respectively, and standard drug sulfasalazine (100 mg/kg, p.o) to group three. Group two served as UC control animals, and group one control animals received vehicle for 7 days. UC was induced by administering AA (3 % v/v of 2 ml) to all the animals except group one. After 72 h, the animals were killed and the colon was dissected out for microscopic, clinical evaluation, histopathological study and biochemical estimation. PM (100 and 200 mg/kg)-treated group had significantly reduced colon inflammation and mucosal damage. The treatment also normalized the altered antioxidant enzyme levels (LPO, SOD and GSH). Histopathological studies support the effect. The protective effect of PM may be due to antiinflammatory and antioxidant properties.