The phytochemical investigation on Vitex negundo leaves has led to the isolation of one new iridoid glucoside (8α-hydroxy-4-carboxyl-5βH-9βH-iridoid-1α-O-(6′-O-(6,7-dihydrofoliamenthonyl)β-ᴅ-glucopyranoside, 3), together with three known compounds, namely agnuside (1), 6′-O-Ecaffeoylmussaenosidic acid (2), and 3,5-dicaffeoylquinic acid (4). The HPLC analytical study was also performed to quantify the content of agnuside (1) in dried leaves. The results indicated the very high content of 1 (3.04 ± 0.02%). The method was also validated by various parameters, including linearity (R 2 = 0.9999), precision (intra-day RSD ≤ 2.50%, inter-day RSD= 0.76%), and accuracy (recovery rates 96.58-101.86%). The animal testing data showed that the extract did not reduce pain at the doses of 9.6 and 28.8 g /kg (leaf weight/body weight) in the hot plates and pain measuring models but showed the pain reduction in the acetic acid-induced pain model. The extract at the dose of 5.6 g/kg (leaf weight/body weight) also had effects on the acute inflammation in the carrageenin-induced edema model. The extract at the dose 9.6 and 28.8 g/ kg (leaf weight/body weight) also showed significant chronic anti-inflammation, comparable to methylprednisolone at the dose 10 mg/kg on the mouse peritoneal.

This study aimed to investigate the neuroprotective and therapeutic effects of Diospyros kaki L.f. leaves (DK) on transient focal cerebral ischemic injury and underlying mechanisms using a middle cerebral artery occlusion (MCAO) model of mice. The animals received the MCAO operation on day 0. The daily administrations of DK (50 and 100 mg/kg, p.o) and edaravone (6 mg/kg, i.v), a reference drug with radical scavenging activity, were started 7 days before (pre-treatment) or immediately after the MCAO operation (post-treatment) and continued during the experimental period. Histochemical, biochemical, and neurological changes were analysed from days 1 to 4, while cognitive performance was evaluated on day 12 after MCAO.MCAO caused cerebral infarction and neuronal cell loss in the cortex, striatum, and hippocampus in a manner accompanied by spatial cognitive de cits. These neurological and cognitive impairments caused by MCAO were signi cantly attenuated by pre-and post-ischemic treatments with DK and edaravone, suggesting that DK, like edaravone, has therapeutic potential for cerebral ischemia-induced brain damage. DK and edaravone suppressed MCAO-induced changes in biomarkers for apoptosis (TUNEL positive cell number and cleaved caspase-3 protein expression) and oxidative stress (glutathione and malondialdehyde contents) in the brain. Interestingly, DK, but not edaravone, mitigated an increase in blood-brain permeability and down-regulation of vascular endothelial growth factor (VEGF)-mediated signalling caused by MCAO. These results indicate that DK exerts neuroprotective and therapeutic activity against transient focal cerebral ischemia-induced injury probably by suppressing oxidative stress, apoptotic process, and mechanisms impairing blood-brain barrier integrity in the brain.

This study aimed to investigate the neuroprotective and therapeutic effects of Diospyros kaki L.f. leaves (DK) on transient focal cerebral ischemic injury and underlying mechanisms using a middle cerebral artery occlusion (MCAO) model of mice. The animals received the MCAO operation on day 0. The daily administrations of DK (50 and 100 mg/kg, p.o) and edaravone (6 mg/kg, i.v), a reference drug with radical scavenging activity, were started 7 days before (pre-treatment) or immediately after the MCAO operation (post-treatment) and continued during the experimental period. Histochemical, biochemical, and neurological changes were analysed from days 1 to 4, while cognitive performance was evaluated on day 12 after MCAO. MCAO caused cerebral infarction and neuronal cell loss in the cortex, striatum, and hippocampus in a manner accompanied by spatial cognitive deficits. These neurological and cognitive impairments caused by MCAO were significantly attenuated by pre- and post-ischemic treatments with DK and edaravone, suggesting that DK, like edaravone, has therapeutic potential for cerebral ischemia-induced brain damage. DK and edaravone suppressed MCAO-induced changes in biomarkers for apoptosis (TUNEL positive cell number and cleaved caspase-3 protein expression) and oxidative stress (glutathione and malondialdehyde contents) in the brain. Interestingly, DK, but not edaravone, mitigated an increase in blood-brain permeability and down-regulation of vascular endothelial growth factor (VEGF)-mediated signalling caused by MCAO. These results indicate that DK exerts neuroprotective and therapeutic activity against transient focal cerebral ischemia-induced injury probably by suppressing oxidative stress, apoptotic process, and mechanisms impairing blood-brain barrier integrity in the brain.

The Chu Lai granitogneiss is widespread throught the Northern Kontum massif. The Chu Lai body is located in the W-SW of the Nui Thanh Townlet (Nui Thanh Dists., Quang Nam Prov.). On an areas of ~ 300 km2. The Chu Lai intrusion mainly consists two mica gneiss, it is light grey and have porphyritic textures. Its major minerals include plagioclase (25÷40%), K-feldpar (20÷40%), quartz (25÷35%), biotite (5÷13%) and mustcovite (0÷6%). Accessory minerals are apatite, zircon, orthit. Garnet and tourmaline are occiasionally found. Zircons separated from a granitogneiss sample colleted in Chu Lai body are generally euhedral to subhedral, dark gray and prissmatic in shape with 100÷300 µm, with length/witdth ratios from 1:1÷1:3. There are many Neoproterozoic - Cambrian ages among the zircon cores in the Chu Lai samples, and these are regarded as inherited zircons. The LA-ICP-MS zircon age is 431 Ma, corresponding to the Silurian. The Chu Lai granitogneiss strongly negative zircon εHf (-4.2÷-11.4) and complex inherited zircon components, characteristics of typical S-type granite. Hf model ages TDM2 1.5÷1.9 Ga, suggests that the Chu Lai granitogneiss was derived from partial melting of old crustal basement rocks, probaly Paleoproterozoic in age.