Alfred Mavondo Greanious, Nkazimulo Mkhwananzi Blessing, Vuyisile Mabandla Musa, Tagumirwa Musabayane Cephas
Discipline of Human Physiology, School of Laboratory Medicine and Medical Sciences, College of Health Sciences, University of KwaZulu Natal, Westville Campus, Durban, 4000, South Africa.
Afr J Tradit Complement Altern Med. 2016 Aug 12;13(5):91-101. doi: 10.21010/ajtcam.v13i5.13. eCollection 2016.
Glucose homeostasis derangement is a common pathophysiology of malaria whose aetiology is still controversial. The parasite, immunological and inflammatory responses, as well as chemotherapeutics currently used cause hypoglycaemia in malaria. Anti-parasitic and anti-disease drugs are required to combat malaria while ameliorating the pathophysiology of the infection. Asiatic acid has anti-hyperglycaemic, antioxidant, pro-oxidant properties useful in glucose homeostasis but its influence in malaria is yet to be reported. Here we present findings on the influence of asiatic acid on glucose metabolism using -infected Sprague Dawley rats.
Acute as well as sub-chronic studies were carried out where physicochemical properties and glucose homeostasis were monitored after administration of asiatic acid (10mg/kg) in both non-infected and infected animals. Glucose metabolism associated biochemical changes in malaria were also investigated.
In acute studies, asiatic acid improved oral glucose response while in the sub-chronic state it maintained food and water intake and suppressed parasitaemia. Normoglycaemic control was maintained in infected animals through insulin suppression and increasing glucagon secretion, in both acute and chronic studies. Asiatic acid administration curtailed lactate concentration towards normal.
Per oral post-infection asiatic acid administration preserved drinking and eating habits, inhibited sickness behaviour while suppressing parasitaemia. Reciprocal relationship between insulin and glucagon concentrations was maintained influencing glucose homeostasis positively and inhibition of hyperlactaemia in malaria. ip -intraperitoneal, po -per oral, ig -intragastric, AA-Asciatic acid, OGTT-oral glucose tolerance test, OS-oxidative stress, ROS-reactive oxygen species, NO-nitric oxide, ONOO - peroxynitrite, BRU-Biomedical Research Unit, SD-Sprague Dawley.
葡萄糖稳态紊乱是疟疾常见的病理生理学表现，其病因仍存在争议。疟原虫、免疫和炎症反应以及目前使用的化疗药物均可导致疟疾患者出现低血糖。在对抗疟疾的同时改善感染的病理生理学，需要抗寄生虫和抗疾病药物。齐墩果酸具有降血糖、抗氧化、促氧化特性，对葡萄糖稳态有益，但其对疟疾的影响尚未见报道。在此，我们展示了齐墩果酸对感染疟原虫的斯普拉格-道利大鼠葡萄糖代谢影响的研究结果。
进行了急性和亚慢性研究，在未感染和感染动物中给予齐墩果酸（10mg/kg）后监测其理化性质和葡萄糖稳态。还研究了疟疾中与葡萄糖代谢相关的生化变化。
在急性研究中，齐墩果酸改善了口服葡萄糖反应，而在亚慢性状态下，它维持了食物和水的摄入量并抑制了寄生虫血症。在急性和慢性研究中，通过抑制胰岛素和增加胰高血糖素分泌，感染动物的血糖正常得以维持。给予齐墩果酸可使乳酸浓度降至正常。
感染后口服齐墩果酸可保持饮食和饮水习惯，抑制疾病行为，同时抑制寄生虫血症。胰岛素和胰高血糖素浓度之间的相互关系得以维持，对葡萄糖稳态产生积极影响，并抑制疟疾中的高乳酸血症。ip -腹腔内注射，po -口服，ig -胃内注射，AA -齐墩果酸，OGTT -口服葡萄糖耐量试验，OS -氧化应激，ROS -活性氧，NO -一氧化氮，ONOO⁻ -过氧亚硝酸盐，BRU -生物医学研究单位，SD -斯普拉格-道利
