Widely used as antipyretics to reduce fever and relieve pain, paracetamol has also been consumed excessively as a means to commit suicide and the incidence is alarming. Paracetamol toxicity as a result of overdose may result in hepatotoxicity and nephrotoxicity. This study was aimed to investigate the therapeutic effects of Cassia alata leaf aqueous extract on protecting and improving kidney morphology of rats exposed to an overdose of paracetamol. 25 male Sprague-Dawley rats were divided equally into five groups: (i) negative control group with standard diet; (ii) positive control group induced with paracetamol toxicity at a dose of 3000 mg/kg rat body weight; (iii) paracetamol-induced (3000 mg/kg) followed by Cassia alata (200 mg/kg) treatment for 21 days; (iv) 21 days treatment of Cassia alata (200 g/kg) followed by paracetamol-induced (3000 mg/kg); and (v) 21 days supplementation of Cassia alata extract only. The rats were sacrificed after treatment is completed to harvest the kidney organ for histological examination via hematoxylin and eosin (H&E) staining. The kidney of positive control rats induced with overdosage of paracetamol demonstrated damaged glomeruli, dilated tubules and endothelial rupture in a capsule. All groups treated with Cassia alata showed improvement in the histological features of kidney morphology, the size of the glomerulus, and the ratio of normal versus damaged glomerulus compared to paracetamol-induced rats. This study concluded that Cassia alata aqueous extract with a dosage of 200 mg/kg are capable to improve kidney morphology damaged by exposure to paracetamol overdose toxicity. � 2018 Pharmascope Publications. All rights reserved.

Retinal ganglion cell (RGC) loss and optic neuropathy, both hallmarks of glaucoma, have been shown to involve N-methyl-D-aspartate receptor (NMDAR)-mediated excitotoxicity. This study investigated the neuroprotective effects of Philanthotoxin (PhTX)-343 in NMDAinduced retinal injury to alleviate ensuing visual impairments. Sprague-Dawley rats were divided into three; Group I was intravitreally injected with phosphate buffer saline as the control, Group II was injected with NMDA (160 nM) to induce retinal excitotoxic injury, while Group III was injected with PhTX-343 (160 nM) 24 h prior to excitotoxicity induction with NMDA. Rats were subjected to visual behaviour tests seven days post-treatment and subsequently euthanized. Rat retinas and optic nerves were subjected to H&E and toluidine blue staining, respectively. Histological assessments showed that NMDA exposure resulted in significant loss of retinal cell nuclei and thinning of ganglion cell layer (GCL). PhTX-343 pre-treatment prevented NMDA-induced changes where the RGC layer morphology is similar to the control. The numbers of nuclei in the NMDA group were markedly lower compared to the control (p<0.05). PhTX-343 group had significantly higher numbers of nuclei within 100 ?m length and 100 ?m2 area of GCL (2.9- and 1.7-fold, respectively) compared to NMDA group (p<0.05). PhTX-343 group also displayed lesser optic nerve fibres degeneration compared to NMDA group which showed vacuolation in all sections. In the visual behaviour test, the NMDA group recorded higher total distance travelled, and lower total immobile time and episodes compared to the control and PhTX-343 groups (p<0.05). Object recognition tests showed that the rats in PhTX-343 group could recognize objects better, whereas the same objects were identified as novel by NMDA rats despite multiple exposures (p<0.05). Visual performances in the PhTX-343 group were all comparable with the control (p>0.05). These findings suggested that PhTX-343 inhibit retinal cell loss, optic nerve damage, and visual impairments in NMDA-induced rats. Copyright � 2020 Fazel et al.