Role of MLC901 in increasing neurogenesis in rats with traumatic brain injury

Rosyidi, Rohadi Muhammad; Priyanto, Bambang; Islam, Andi Asadul; Hatta, Mochammad; Bukhari, Agussalim; Prihastomo, Krisna Tsaniadi; Nasution, Rizha Anshori; Rozikin,; Prihatina, Lale Maulin

doi:10.1016/j.amsu.2020.10.013

Cited by 6 publications

(5 citation statements)

References 22 publications

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“…Preclinical study of MLC901 administration (NeuroAiD II) can increase number of neuronal cell (neurogenesis) in a rat model with brain injury [16].…”

Section: Discussionmentioning

confidence: 99%

Untitled

2022

Neurosurg Cases Rev

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Traumatic brain injury (TBI) is a major cause of mortality and morbidity worldwide. The medical management of TBI involves stabilization of the individual and focusing on preventing further injury. There are no proven pharmacological therapies to enhance recovery after severe TBI.We present case reports of two patients who had severe head injury due to a motor vehicular accident, taken from the NeuroAiDSafe Treatment (NeST) Registry, which is a prospective, real world data registry initiated to monitor the use and safety of the NeuroAiD in various clinical indications. The computerized tomography (CT) brain scan of both patients showed multiple intracranial haemorrhages, subdural and contusion hematoma. Both cases required resuscitative care and ventilatory support management in the intensive care unit and subsequent medical management including intensive rehabilitation. MLC601 (NeuroAiD) was started after 3 weeks and 11 days for patients 1 and 2, respectively. Improvement in the Glasgow Coma Scale (GCS), motor and sensory functions were noted as early as one month with gradual improvement by 3rd and 6th month. There was a residual slurred speech and partial gaze paresis noted in the first patient, while the other had a full recovery. There were no adverse events reported related to MLC601. NeuroAiD may play a role in enhancing recovery after severe traumatic brain injury.

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“…Preclinical study of MLC901 administration (NeuroAiD II) can increase number of neuronal cell (neurogenesis) in a rat model with brain injury [16].…”

Section: Discussionmentioning

confidence: 99%

Untitled

2022

Neurosurg Cases Rev

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“…SCIbased research requires a highly efficient and easily reproducible animal model, which can help in limiting inconclusive data [18]. The traditional method of inducing injury requires different impactors such as New York University [18], Infinite horizon [13], Ohio State University [20], Air gun impactor etc. which are extremely expensive and their availability is limited [5].…”

Section: Discussionmentioning

confidence: 99%

“…Glutamate excitotoxicity neuronal injury models are simple and reliable. Glutamate excitotoxicity is triggered primarily due to excessive Ca 2+ influx, endoplasmic reticulum (ER) membrane disintegration and ER stress, reactive oxygen species [13] production, mitochondrial dysfunction, neuronal cells apoptosis [3]. A potent agonist of the AMPA/kainate class of glutamate receptors, KA is a non-degradable analogue of glutamate and causes 30 times more potent neurotoxicity than glutamate [11].…”

Section: Introductionmentioning

confidence: 99%

Protocol paper: kainic acid excitotoxicity-induced spinal cord injury paraplegia in Sprague–Dawley rats

et al. 2022

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Background Excitotoxicity-induced in vivo injury models are vital to reflect the pathophysiological features of acute spinal cord injury (SCI) in humans. The duration and concentration of chemical treatment controls the extent of neuronal cell damage. The extent of injury is explained in relation to locomotor and behavioural activity. Several SCI in vivo methods have been reported and studied extensively, particularly contusion, compression, and transection models. These models depict similar pathophysiology to that in humans but are extremely expensive (contusion) and require expertise (compression). Chemical excitotoxicity-induced SCI models are simple and easy while producing similar clinical manifestations. The kainic acid (KA) excitotoxicity model is a convenient, low-cost, and highly reproducible animal model of SCI in the laboratory. The basic impactor approximately cost between 10,000 and 20,000 USD, while the kainic acid only cost between 300 and 500 USD, which is quite cheap as compared to traditional SCI method. Methods In this study, 0.05 mM KA was administered at dose of 10 µL/100 g body weight, at a rate of 10 µL/min, to induce spinal injury by intra-spinal injection between the T12 and T13 thoracic vertebrae. In this protocol, detailed description of a dorsal laminectomy was explained to expose the spinal cord, following intra-spinal kainic acid administration at desired location. The dose, rate and technique to administer kainic acid were explained extensively to reflect a successful paraplegia and spinal cord injury in rats. The postoperative care and complication post injury of paraplegic laboratory animals were also explained, and necessary requirements to overcome these complications were also described to help researcher. Results This injury model produced impaired hind limb locomotor function with mild seizure. Hence this protocol will help researchers to induce spinal cord injury in laboratories at extremely low cost and also will help to determine the necessary supplies, methods for producing SCI in rats and treatments designed to mitigate post-injury impairment. Conclusions Kainic acid intra-spinal injection at the concentration of 0.05 mM, and rate 10 µL/min, is an effective method create spinal injury in rats, however more potent concentrations of kainic acid need to be studied in order to create severe spinal injuries.

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“…All surgical procedures were performed aseptically by adhering to the principle of sterility. After the surgery and trauma, all animals were kept at room temperature for recovery and returned to their cages according to their groups [ 20 , 27 , 28 , 30 ].…”

Section: Methodsmentioning

confidence: 99%

“…MLC 901 has neuroprotective and neuroproliferative effects and has been extensively described during in vitro and in vivo experiments using animal models. The remarkable effect of MLC 901 lies in its neurogenesis and neurorestoration effects rather than its neuroprotective effects [ [25] , [26] , [27] ].…”

Section: Introductionmentioning

confidence: 99%