Terminalia arjuna bark extract attenuates picrotoxin-induced behavioral changes by activation of serotonergic, dopaminergic, GABAergic and antioxidant systems.

Stress and emotion are associated with several illnesses from headaches to heart diseases and immune deficiencies to central nervous system. Terminalia arjuna has been referred as traditional Indian medicine for several ailments. The present study aimed to elucidate the effect of T. arjuna bark extract (TA) against picrotoxin-induced anxiety. Forty two male Balb/c mice were randomly divided into six experimental groups (n = 7): control, diazepam (1.5 mg·kg-1), picrotoxin (1 mg·kg-1) and three TA treatemt groups (25, 50, and 100 mg/kg). Behavioral paradigms and PCR studies were performed to determine the effect of TA against picrotoxin-induced anxiety. The results showed that TA supplementation increased locomotion towards open arm (EPM) and illuminated area (light-dark box test), and increased rearing frequency (open field test) in a dose dependent manner, compared to picrotoxin (P < 0.05). Furthermore, TA increased number of licks and shocks in Vogel's conflict. PCR studies showed an up-regulation of several genes, such as BDNF, IP3, D2L, CREB, GABAA, SOD, GPx, and GR in TA administered groups. In conclusion, alcoholic extract of TA bark showed protective activity against picrotoxin in mice by modulation of genes related to synaptic plasticity, neurotransmitters, and antioxidant enzymes.

Antidepressant like effects of hydrolysable tannins of Terminalia catappa leaf extract via modulation of hippocampal plasticity and regulation of monoamine neurotransmitters subjected to chronic mild stress (CMS).

Terminalia catappa L. belonging to Combretaceae family is a folk medicine, known for its multiple pharmacological properties, but the neuro-modulatory effect of TC against chronic mild stress was seldom explored. The present study was designed to elucidate potential antidepressant-like effect of Terminalia cattapa (leaf) hydro-alcoholic extract (TC) by using CMS model for a period of 7 weeks. Identification of hydrolysable tannins was done by using LC-MS. After the CMS exposure, mice groups were administered with imipramine (IMP, 10mg/kg, i.p.) and TC (25, 50 and 100mg/kg of TC, p.o.). Behavioural paradigms used for the study included forced swimming test (FST), tail suspension test (TST) and sucrose preference test (SPT). After behavioural tests, monoamine neurotransmitter, cortisol, AchE, oxidative stress levels and mRNA expression studies relevant to depression were assessed. TC supplementation significantly reversed CMS induced immobility time in FST and other behavioural paradigms. Moreover, TC administration significantly restored CMS induced changes in concentrations of hippocampal neurotransmitters (5-HT, DA and NE) as well as levels of acetyl cholinesterase, cortisol, monoamine oxidases (MAO-A, MAO-B), BDNF, CREB, and p-CREB. It suggests that TC supplementation could supress stress induced depression by regulating monoamine neurotransmitters, CREB, BDNF, cortisol, AchE level as well as by amelioration of oxidative stress. Hence TC can be used as a complementary medicine against depression-like disorder.

Effect of bacoside extract from Bacopa monniera on physical fatigue induced by forced swimming.

The antifatigue effect of bacoside extract (BME) from Bacopa monniera (L.) Wettst. was investigated. Rats were subjected to weight-loaded forced swim test (WFST) every alternate day for 3 weeks. The BME at a dosage of 10 mg/kg body weight was administered orally to rats for 2 weeks in order to evaluate the following biomarkers of physical fatigue: swimming time, change in body weight, lipid peroxidation, lactic acid (LA), glycogen, antioxidant enzyme activities such as superoxide dismutase (SOD) and catalase (CAT) and blood parameters, namely blood urea nitrogen (BUN) and creatine kinase (CK). The exhaustive swimming time was increased by 3-fold in the BME supplemented group compared with that of the control group on day 13. The BME treatment lowered malondialdehyde (MDA) levels in brain, liver and muscle tissues by 11.2%, 16.2% and 37.7%, respectively, compared with the control exercised group (p < 0.05). The BME also reduced the LA, serum BUN and CK activities significantly compared with that of the control. Administration of BME significantly protected the depletion of SOD and CAT activities. The HSP-70 expression studies by western blot also confirmed the antifatigue property of BME. The present study thus indicates that BME ameliorates the various impairments associated with physical fatigue.