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Objective: An extract (Methanolic) of the Ocimum basilicum leaf was analysed for potential to abrogate experimental formation of cataract in-vitro. Methods: Phytoconstituents were first detected in O. basilicum extracts (Aqueous or methanolic) by gas chromatographic-mass spectrometric analysis. The putative antioxidant activity of these extracts was then assessed by measuring in-vitro radical-scavenging activity, ion-chelating potential and reducing potency. Potential cytotoxicity of the extract on Human lenticular epithelial B3 (HLE-B3) cells was also sought. Finally, possible prevention of cataract formation by the methanolic extract was gauged in selenite-exposed lenses obtained from Wistar rats. There were 3 groups (8 Lenses in each): Group I (Lenses incubated in Dulbecco’s modified Eagle’s medium [DMEM] alone); Group II (Lenses incubated in DMEM with sodium selenite [100 μM/ml]); Group III (Lenses incubated in DMEM with selenite [100 μM/ml] and the O. basilicum methanolic extract (200 μg/ml DMEM). Gross lenticular morphology was assessed. Levels of lenticular malondialdehyde (MDA) and reduced glutathione (GSH) were also measured. Results: A higher intensity of antioxidative activity was noted in the methanolic extract than in the aqueous extract. The methanolic extract exhibited negligible cytotoxicity. On morphological examination, marked opacification was seen in all 8 Group II lenses whereas there was no opacification in 7 of 8 Group III lenses. Near normal mean levels of reduced glutathione and malondialdehyde, were noted within Group III lenses. Conclusion: The methanolic extract of the O. basilicum leaf appears to prevent selenite-induced cataract formation in-vitro. [ABSTRACT FROM AUTHOR]

Background: Combinations of the traditional Chinese and Western medicines have been used to treat numerous diseases throughout the world, and there is a growing body of evidence showing that some of the herbs used in traditional Chinese medicine elicit signiicant pharmacological effects. The aim of this study was to demonstrate the neuroprotective efects of Tao-Ren-Cheng-Qi Tang (TRCQT) in combination with aspirin following middle cerebral artery occlusion (MCAO)--induced embolic stroke in rats. Methods: A blood clot was embolized into the middle cerebral artery of rats to induce focal ischemic brain injury. After 24 h of MCAO occlusion, the rats were arbitrarily separated into five groups and subjected to diferent oral treatment processes with TRCQT and aspirin for 30 days before being evaluated in terms of their neurological behavior using a four-point system. The rats were sacrificed at 30 days after drug treatment and the infarct volumes were measured using a 2,3,5-triphenyltetrazolium chloride staining method. Tumor necrosis factor-α (TNF-α), c-Jun N-terminal kinases (JNK), activated caspase-3 and Bax were detected by western blot analysis. The apoptotic cells were identified by Terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) staining. ROS generation was also measured by electron spin resonance spectrometry. Results: Rats treated with TRCQT alone or in combination with aspirin showed a signiicantly reduced infarct volume (P < 0.001) and improved neurological outcome compared with those treated with distilled water. Rats treated with TRCQT alone (P = 0.021) or in combination with aspirin (P = 0.02) also showed signiicantly reduced MCAO-induced expression levels of TNF-α and pJNK (P < 0.001) in their ischemic regions. Rats treated with TRCQT alone or in combination with aspirin showed decreased apoptosis by a reduction in the number of TUNEL positive cells, which inhibited the expression of activated caspase-3 (P = 0.038) and Bax (P = 0.004; P = 0.003). TRCQT also led to a significant concentration-dependent reduction in the formation of hydroxyl radicals (P < 0.001). Conclusions: TRCQT reduced brain infarct volume and improved neurological outcomes by reducing apoptosis, attenuating the expression of TNF-α and p-JNK, and reducing the formation of hydroxyl radicals in MCAO-induced embolic stroke of rats. [ABSTRACT FROM AUTHOR]