Fenugreek with the scientific name of Trigonella foenum-graceum L and with leaves consisting of 3 small obovate to oblong leaflets is an annual herbaceous plant of the Fabaceae family. It is native to the eastern Mediterranean but is cultivated worldwide. This plant has medicinal alkaloids, steroid compounds, and sapogenins and many uses have been mentioned for this plant in traditional medicine. This plant has been used to ease childbirth, to aid digestion, and as a general tonic to improve metabolism. Trigonelline is considered as the most important metabolite of fenugreek, which is very effective in treating diabetes and decreasing blood cholesterol. Diaszhenin is another important compound in seeds of this plant, which is used in producing medicinal steroids like contraceptive pills. Many studies have been performed on the therapeutic effects and identification of chemical compounds of this plant. In this article, the most important biological effects and reported compounds about fenugreek seed are reviewed and its therapeutic applications are investigated.

AbstractBackgroundInterferon-α (IFNα) therapy causes psychiatric side effects, including depression that may result in poor compliance of therapy. It is important to find alternative therapies for the prevention of IFNα induced depression. Non-steroidal anti-inflammatory drugs (NSAIDs) have been useful in depressive disorder. Therefore the effects of celecoxib, ibuprofen, and indomethacin were evaluated following IFNα-induced depression in mice.MethodsMale albino mice weighing 26 ± 2 g were used. Depression was induced by IFNα (16 × 105 IU/kg, SC) for six consecutive days. Animals were first subject to the locomotor test, then the splash test and finally the forced swimming test (FST) on the 7th day. The NSAIDs were administered (IP) either one single dose before the test, or simultaneously with IFNα.Resultslocomotor activity was only impaired by ibuprofen high dose (75 mg/kg), thus it was not further evaluated. Following IFNα therapy depression-like behaviors were observed; significant changes during the splash test (grooming time 24 ± 7 sec vs. control 63 ± 7 sec), the FST (immobility time 166  ± 15 sec vs. control 128  ± 6 sec), and sucrose preference reduced to 64 ± 0.8%. The NSAIDs noticeably reduced the immobility time in FST, while grooming time was increased. Celecoxib and indomethacin single doses were effective while ibuprofen showed better antidepressant effects when it was administered along with IFNα.ConclusionsThe NSAIDs were able to prevent IFNα induced depression in mice. NSAIDs administration with IFNα does not interfere with clinical benefit effects of IFNα and they could also be useful to prevent IFNα psychiatric side effects, thus further clinical trials are suggested.

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Glucocorticoid hormones evidently affect memory. Morphine withdrawal causes a cognitive deficit and an increase in corticosterone secretion. In the present study brain corticosterone concentrations were determined after morphine withdrawal. Male mice were made dependent by increasing doses of morphine over 3 days. Blood and brain samples were collected following withdrawal induced by injection of naloxone (0.1 mg/kg) or spontaneously after 4 and 14 h. Brain corticosterone was extracted and measured by enzyme immunoassay. Short-term memory was determined in the novel object recognition task, using a 20 min interval between the learning trial and the test trial. In this memory trial, the difference in exploration between a previously seen object and a novel object is taken as an index of memory performance (recognition index, RI). RI in morphine dependent mice undergoing withdrawal was decreased compared to their control group. Brain corticosterone concentrations after naloxone withdrawal or 4 h after spontaneous withdrawal were respectively 22 and 34% greater than control values. Corticosterone concentration was normalized 14 h after the last dose of morphine. The results indicate that increase in brain corticosterone concentration may play an important role in short-term memory impairment following morphine withdrawal.

Vitamin B6 prevented DEX-induced depression possibly by altering the GR function. Thus Vitamin B6 could be promising in patients suffering from GC-induced psychiatric adverse effects and probably controlling stress and preventing its affective disorder out comes.