Kemerosotan kesihatan otak merupakan suatu wabak di seluruh dunia. Penyakit Alzheimer dan demensia lain adalah antara penyakit yang tertinggi kos untuk dirawat, dengan perbelanjaan penjagaan langsung melebihi mereka yang menghidap kanser dan penyakit jantung. Pengambilan terlalu banyak dan terlalu kerap produk makanan terproses telah menyumbang kepada peningkatan kemerosotan kesihatan pada usia yang muda. Madu telah diketahui di seluruh dunia sejak sekian lama merupakan salah satu produk asli dan semulajadi untuk digunapakai sebagai makanan kesihatan terutamanya disebabkan oleh kandungan antioksidan dan fenoliknya. Beberapa dekad kebelakangan ini, banyak kajian telah dilakukan untuk memahami proses biologi gangguan kerosakan terhadap sel otak dan cara untuk menghentikan atau melambatkan proses berkenaan menggunakan produk semulajadi. Madu telah menunjukkan potensi besar yang mampu mengurangkan atau melambatkan gangguan kemerosotan saraf ini. Berdasarkan kajian terbaru penggunakan madu dan kesannya ke atas anatomi dan fisiologi otak, menunjukkan bahawa madu mempunyai potensi untuk menghentikan atau merawat gangguan kemerosotan kesihatan otak.

Objective: To explore the protective effect of Polygonum minus ethanolic extract on cisplatin-induced neurotoxicity. Methods: In vitro test, total phenolic content assay and DPPH assay were performed to determine the antioxidant activity of Polygonum minus. For in vivo test, 30 male Sprague-Dawley rats were randomly divided into 5 groups: the control group, cisplatin 10 mg/kg, Polygonum minus 100 mg/kg, Polygonum minus 200 mg/kg and Polygonum minus 400 mg/kg. The control group and the cisplatin group were given distilled water whereas Polygonum minus groups received the respective dose of Polygonum minus extract orally for 14 d. On day 15, a single intraperitoneal administration of normal saline was given to the control group; while 10 mg/kg of cisplatin was given to the cisplatin group and Polygonum minus groups. Body weight, signs of illness, daily activity and mortality were observed at least once daily throughout the experimental period. On day 18, the anterior part of the brain was collected and processed for histological and ultrastructural analyses (right hemisphere). The remaining part (left hemisphere) of the brain was assayed to determine malondialdehyde and catalase levels for oxidative stress analyses. Results: Polygonum minus ethanolic extract possessed high phenolic content (977.6 mg GAE/g) and 95.9％ DPPH radical scavenging activities. No mortality was observed in all groups. Rats in the cisplatin group were weak and less active compared to Polygonum minus treated rats. In the cisplatin group, disorganised cellular layers of the cerebral cortex were observed whereas rats treated with low and mid doses of Polygonum minus extract had normal cerebral cortex as in the control group. Mild ultrastructural changes were observed in rats treated with low and mid doses of Polygonum minus extract. Meanwhile, low and mid doses of Polygonum minus extract significantly reduced malondialdehyde level whereas low and mid doses of Polygonum minus extracts groups significantly increased catalase activity compared to the cisplatin group. Conclusions: Polygonum minus ethanolic extract at 100 and 200 mg/kg attenuates cisplatin-induced oxidative stress in the cerebral cortex via its antioxidant activity.

The occurrence of severe lead (Pb) poisoning has risen in certain countries. There is increasing evidence that chronic lead exposure disturbs the prooxidant: antioxidant balance in the brain tissue and alters brain histology. The present study observed the antioxidant effect of tocotrienol-rich fraction (TRF) on brain tissues of the experimental rats following lead poisoning. Eighteen (n=18) male Sprague-Dawley rats, 6-weeks old, were randomly divided into control (CTRL) group and experimental groups; fed with 0.2% w/v lead acetate, as PB2 group; and fed with 0.2% w/v lead acetate and daily TRF supplementation (200 mg/kg body weight) as PB2T group. The experiment was conducted for 30 days. At the end of the study, the brain tissues were harvested and histopathological changes of the hippocampal region were observed. Biochemical findings such as brain lead, TRF and malondialdehyde (MDA) levels, and erythrocyte superoxide dismutase (SOD) activity were determined. It was observed that atypical apoptotic-like and disorganized neurons were present in the hippocampal region of the untreated PB2 group compared to PB2T group. Biochemical parameters showed a significant decrease (p < 0.05) in brain lead level in PB2T compared to PB. Even though no significant difference (p > 0.05) was obtained for MDA level, there was a significant increase (p < 0.05) in the erythrocyte SOD activity in PB2T compared to PB2 and CTRL. Supplementation with TRF improved histopathological changes in the brain tissues caused by lead exposure in drinking water by reducing lead accumulation in the brain of experimental rats.
Lead Poisoning

Delayed wound healing is one of the major complications of diabetes mellitus where it often leads to amputation. Virgin coconut oil (VCO) is a natural oil widely used to treat wounds and burns traditionally. It possesses potent antioxidant and antibacterial activities. This study aimed to determine the effect of VCO on the fibroblast population in diabetic wound healing. Full thickness cutaneous wound tissues were collected from non-treated, VCO-treated, and silver sulfadiazine (SS)-treated diabetic rats. The tissues were then subjected to Verhoeff eosin staining and immunohistology of fibroblast and myofibroblast. Histological analysis showed increased collagen deposition with intact epidermis in the VCO treated group compared to decreased collagen deposition with damaged epidermis in both non-treated and SS-treated groups. Interestingly, more fibroblasts and myofibroblasts were observed in the non-treated group compared to the VCO- and SS-treated groups. VCO significantly promoted wound healing process in diabetic rats via promoting re-epithelialization, and increasing collagen fibres deposition and wound contraction. The results suggested VCO can be used to treat diabetic wounds.

Long term glucocorticoids administration induces oxidative stress which leads to alteration of bone structure and strength. Palm oil is rich in tocotrienol, an antioxidant. It can be used for the prevention of oxidative stress related diseases. The main objective of this study was to determine the mechanism of palm tocotrienol in maintaining the bone structure and strength in glucocorticoid-induced osteoporosis. Thirty two adult male Sprague-Dawley rats, aged 3 months, weighing 300-320 g rats were used in this study. Sixteen rats undergone adrenalectomy and were administered with 120μg/kg/day intramuscular injection of dexamethasone. Eight rats were supplemented with oral palm tocotrienol 60 mg/kg/day (Adrx+Dex+PTT) and the other eight rats were given oral vehicle palm olein 0.1 ml/kg/day (Adrx+Dex). Eight rats underwent sham procedure and were given vehicle palm olein 0.05 ml/kg/day by intramuscularly and oral 0.1 ml/kg/day (Sham). The rats were euthanized after two months of treatments. Eight rats were euthanized after acclimatic action without receiving any treatment (Baseline). The right femurs were used for bone biomechanical strength and histomorphometry analysis while the left for gene expression and oxidative stress enzymes activities. The results indicated that long-term glucocorticoid treatment significantly increased bone resorption marker, CTX (6060.7 ± 410 pg/ml) and decreased bone structure and strength. Osteoblast and osteoclast related genes expressions indicated an increase in bone turnover. Supplementation of palm tocotrienol had maintained serum resorption (2619.4 + 209 pg/ml) marker level and preserved bone structure and strength. Gene expression analysis showed decrease in bone resorption. The findings suggested that palm tocotrienol has potential benefits against glucocorticoid-induced osteoporosis by regulating osteoblast and osteoclast related gene expression