Rasayana tantra is one of the eight specialties of Ayurveda. It is a specialized practice in the form of rejuvenative recipes, dietary regimen, special health promoting behaviour and drugs. Properly administered Rasayana can bestow the human being with several benefits like longevity, memory, intelligence, freedom from diseases, youthful age, excellence of luster, complexion and voice, optimum strength of physique and sense organs, respectability and brilliance. Various types of plant based Rasayana recipes are mentioned in Ayurveda. Review of the current literature available on Rasayanas indicates that anti-oxidant and immunomodulation are the most studied activities of the Rasayana drugs. Querying in Pubmed database on Rasayanas reveals that single plants as well as poly herbal formulations have been researched on. This article reviews the basics of Rasayana therapy and the published research on different Rasayana drugs for specific health conditions. It also provides the possible directions for future research.
Animals ; Anti-Ulcer Agents ; pharmacology ; therapeutic use ; Antineoplastic Agents, Phytogenic ; pharmacology ; therapeutic use ; Antiparasitic Agents ; pharmacology ; therapeutic use ; Aphrodisiacs ; pharmacology ; therapeutic use ; Free Radical Scavengers ; pharmacology ; therapeutic use ; Giardiasis ; drug therapy ; Herbal Medicine ; classification ; methods ; trends ; Humans ; Immunologic Factors ; pharmacology ; therapeutic use ; Medicine, Ayurvedic ; Models, Biological ; Neuroprotective Agents ; pharmacology ; therapeutic use ; Plant Preparations ; classification ; therapeutic use ; Radiation-Protective Agents ; pharmacology ; therapeutic use

Survival rates after cardiac arrest have not changed substantially over the past 5 decades. Postcardiac arrest (CA) syndrome (PCAS) is the primary reason for the high mortality rate after successful restoration of spontaneous circulation (ROSC). Intravenous administration of Shenfu Injection (, SFI) may attenuate post-CA myocardial dysfunction and cerebral injury, inhibit systemic ischemia/reperfusion responses, and treat underlying diseases. In this article, we reviewed the therapeutic effects of SFI in PCAS. SFI might be useful in the treatment of PCAS, incorporating the multi-link and multi-target advantages of Chinese medicine into PCAS management. Further experimental and clinical research to verify the therapeutic effects of SFI in PCAS is required.
Cardiotonic Agents ; pharmacology ; therapeutic use ; Drugs, Chinese Herbal ; administration & dosage ; therapeutic use ; Heart Arrest ; drug therapy ; physiopathology ; Humans ; Injections ; Neuroprotective Agents ; pharmacology ; therapeutic use ; Syndrome

Baicalein, a flavonoid compound extracted from dried roots of traditional Chinese medicine Scutellaria baicalensis, has been widely applied as an antioxidant and anti-inflammatory agent. With continuous studies on its mechanisms, recent findings suggest that baicalein has some effect on neuroprotection and improvement of clinical symptoms in neurodegenerative diseases such as Parkinson's disease. Recent studies showed that its neuroprotective efficacy is closely related to such functions as antiinflammatory, antioxidative stress, protecting chondriosome, inhibiting glutamate neurotoxicity, promoting nerve growth and inhibiting alpha-synuclein protein-aggregate activities. The aim of this article is to summarize the neuroprotective effects of baicalein in Parkinson's disease.
Flavanones ; pharmacology ; therapeutic use ; Humans ; Mitochondria ; drug effects ; metabolism ; Nerve Growth Factor ; metabolism ; Neuroprotective Agents ; pharmacology ; therapeutic use ; Oxidative Stress ; drug effects ; Parkinson Disease ; drug therapy ; metabolism ; pathology

OBJECTIVETo explore the neuroprotective effect of FK506 on acute spinal cord injury in dogs.

METHODSAcute spinal cord injury model was made with the Allen technique. Animals were randomly divided into 3 groups. Group A (n = 8) was the control group and received operation but no therapy, while group B and C (n = 8) received a single dose of FK506 (0.18 mg/kg and 0.3 mg/kg, respectively) administered with an arterial duct 2 h after spinal cord injury (SCI). Spine MRI, neurological function, histopathological examination of injured spinal cord and immunohistochemical examination of expression of NF(200) in neurons and GFAP in astrocytes were assessed at certain time after injury.

RESULTSNeurological function score of group C and B was better than that of group A (P < 0.05), with significance between group C and A, while no significance between group B and A statistically. The signal scope of spinal cord injury on MRI in group C was the smallest among all the groups, and the signal scope in group B was smaller than that in group A, which was directively associated with the neurological outcome. The expression of NF and GFAP was significantly higher in group C than in group A (P < 0.05), but without statistical significance between group B and A.

CONCLUSIONLocal administration of FK506 (0.3 mg/kg) possesses neuroprotective effect on acute spinal cord injury, which can improve neurological function recovery and attenuate secondary spinal cord injury. Local administration of FK506 possesses a dosage-effect relation.

Acute Disease ; Animals ; Disease Models, Animal ; Dogs ; Female ; Male ; Neuroprotective Agents ; pharmacology ; therapeutic use ; Random Allocation ; Spinal Cord Injuries ; drug therapy ; Tacrolimus ; pharmacology ; therapeutic use

Contemporary pharmacological research has demonstrated that puerarin, the most important phytoestrogen extracted from Pueraria lobata(Willd.) Ohwi, has protecting functions on the cardiovascular system, nervous system, osteoporosis, liver injury, and inflammation in vivo and in vitro. Most of these research studies focused on inhibiting oxidative stress and apoptosis through regulating various bioactivators and signal pathways. Among these, superoxide dismutase (SOD), endothelial nitric oxide synthase (eNOS) and malondialdehyde (MDA), and PI3K/Akt, MAPK, and NF-κB are of great importance. The data cited in this review were mainly obtained from articles listed in PubMed and Elsevier SDOL published from 1959 to 2013, and the search term used was "puerarin".
Anti-Inflammatory Agents ; pharmacology ; therapeutic use ; Antioxidants ; pharmacology ; therapeutic use ; Apoptosis ; drug effects ; Cardiovascular Diseases ; prevention & control ; Humans ; Isoflavones ; pharmacology ; therapeutic use ; Liver Diseases ; prevention & control ; Neuroprotective Agents ; pharmacology ; therapeutic use ; Oxidative Stress ; drug effects ; Phytoestrogens ; pharmacology ; therapeutic use ; Phytotherapy ; Plant Extracts ; pharmacology ; therapeutic use ; Pueraria ; chemistry

OBJECTIVETo investigate the neuroprotective effects of glycyrrhizin (Gly) as well as its effect on expression of high-mobility group box 1 (HMGB1) in rats after traumatic brain injury (TBI).

METHODSMale Sprague-Dawley rats were randomly divided into three groups: sham group, TBI group, and TBI+Gly group (n=36 per group). Rat TBI model was made by using the modified Feeney's method. In TBI+Gly group, Gly was administered intravenously at a dosage of 10 mg/kg 30 min after TBI. At 24 h after TBI, motor function and brain water content were evaluated. Meanwhile, HMGB1/HMGB1 receptors including toll-like receptor 4 (TLR4) and receptor for advanced glycation end products (RAGE)/nuclear factor-κB(NF-κB) signaling pathway and inflammatory cytokines in the injured brain tissues were detected using quantitative real-time polymerase chain reaction, western blot, electrophoretic mobility shift assay and enzyme-linked immunosorbent assay. Furthermore, HMGB1, RAGE and TLR4 immunohistochemistry and apoptosis were analyzed.

RESULTSBeam walking performance impairment and brain edema were significantly reduced in TBI+Gly group compared with TBI group; meanwhile, the over-expressions of HMGB1/HMGB1 receptors (TLR4 and RAGE)/NF-κB DNA-binding activity and inflammatory cytokines were inhibited. The percentages of HMGB1, RAGE and TLR4-positive cells and apoptotic cells were respectively 58.37% ± 5.06%, 54.15% ± 4.65%, 65.50% ± 4.83%, 52.02% ± 4.63% in TBI group and 39.99% ± 4.99%, 34.87% ± 5.02%, 43.33% ± 4.54%, 37.84% ± 5.16% in TBI+Gly group (all P<0.01 compared with TBI group).

CONCLUSIONGly can reduce secondary brain injury and improve outcomes in rat following TBI by down-regulation of HMGB1/HMGB1 receptors (TLR4 and RAGE)/NF-κB-mediated inflammatory responses in the injured rat brain.

Animals ; Brain Injuries ; drug therapy ; Glycyrrhizic Acid ; pharmacology ; therapeutic use ; HMGB1 Protein ; metabolism ; Male ; Neuroprotective Agents ; therapeutic use ; Rats ; Rats, Sprague-Dawley

OBJECTIVEThe brain damage caused by repeated febrile seizure (FS) during developing age is harmful to the intellectual development of children. So how to decrease the related damage is a very important issue. The main purpose of the present study was to find out whether the non-specific opiate antagonist naloxone at low dose has the neuroprotective effect on seizure-induced brain damage.

METHODSWarm water induced rat FS model was developed in this study. Forty-seven rats were randomly divided into two groups: normal control group (n = 10) and hyperthermic seizure groups (n = 37). The latter was further divided into FS control group (n = 13) and naloxone-treated group (n = 24). The dose of naloxone is different in two naloxone-treated groups (12/each group), in one group the dose was 1 mg/kg, in the other one 2 mg/kg. Seven febrile seizures were induced in each rat of hyperthermic seizure groups with the interval of 2 days. The rats were weighed and injected intraperitoneally with naloxone once the FS occurred in naloxone-treated group, while the rats of the other groups were injected with 0.9% sodium chloride. Latency, duration and grade of FS in different groups were observed and compared. HE-staining and the electron microscopy (EM) were used to detect the morphologic and ultrastructural changes of hippocampal neurons.

RESULTSIn naloxone-treated group, the rats' FS duration and FS grade (5.02 +/- 0.63, 2.63 +/- 0.72) were significantly lower (t = 5.508, P < 0.01; t = 8.439, P < 0.01) than those in FS control group (7.70 +/- 2.25 min, 4.52 +/- 0.49), although no significant gap was observed on FS latency between them. In FS control group, HE-staining pattern of hippocampal CA(1) and CA(2) showed lots of disordered neurons with confused polarity and vacuoles formed. Nuclei were with various size, some rounded and some oblong. While in naloxone-treated groups, the arrangement of neurons was regular, only a small quantity of neurons had changed polarity and vacuoles formed. Most nuclei were oblong and in the same size. In hippocampal CA(1) region and dentate gyrus of rats from FS control group, EM showed that the most mitochondrion volumes obviously increased with vacuoles formed, the matrix condensed, the ridge obscured or disappeared, apoptosis body emerged. Minor to moderate dilation of rough endoplasmic reticulum and Golgi's complex was also observed. However, in naloxone-treated groups, the number of neurons with swollen mitochondrion and endoplasmic reticulum was much fewer than that in FS control group. No apoptosis body was observed. The comparison between them showed much lighter brain damage in naloxone-treated groups than in FS control group.

CONCLUSIONAlthough low-dose naloxone could not totally stop the occurrence of febrile seizure, it could lighten the brain damage resulted from repeated FS to some extent.

Animals ; Brain ; drug effects ; pathology ; Male ; Models, Animal ; Naloxone ; pharmacology ; therapeutic use ; Narcotic Antagonists ; pharmacology ; therapeutic use ; Neuroprotective Agents ; pharmacology ; therapeutic use ; Random Allocation ; Rats ; Rats, Sprague-Dawley ; Seizures, Febrile ; drug therapy ; physiopathology ; Treatment Outcome

OBJECTIVETo explore the regulatory effect of Suifukang (SFK), a compound Chinese patent drug on the change of free radical in tissue of spinal cord and blood caused by experimental spinal injury.

METHODSSeventy male adult SD rats were randomly divided into 4 groups, the SFK group (n = 20), the hormone group (n = 20), the control group (n = 20) and the normal group (n = 10). Rats in the former three groups were made into the right hemitransected spinal cord (T12) injury. SFK were given to the rats in the SFK group 3 days before and 2 hrs after modeling via gastrogavage, saline was given to rats in the control group at the same time. As for the rats in the hormone group, methyl-prednisolone 30 mg/kg was given once immediately by peritoneal injection. The rats were sacrificed in two batches (10 of each group in each batch) at 8 hrs and 24 hrs after modeling to obtain the serum and injured spinal cord tissue for determining superoxide dismutase (SOD) activity and malondialdehyde (MDA) content.

RESULTS(1) As compared with the normal group, SOD activity in serum and spinal tissue of the control group was lower significantly both at 8 hrs and 24 hrs after modeling, but the changes of SOD activity in the SFK and the hormone group were insignificant; (2) Content of MDA in serum and spinal tissue of rats elevated after modeling, which in the control group at 8 hrs after modeling were higher than that in the normal group, also higher than that in the SFK group and the hormone group; but at 24 hrs after modeling, it lowered significantly in both treated groups. The changes of MDA content in serum were similar to those in the spinal tissue.

CONCLUSIONSFK could effectively eliminate the excessive free radical in serum and injured spinal tissue, and raise the capability of antioxidation of organism.

Animals ; Drugs, Chinese Herbal ; pharmacology ; therapeutic use ; Free Radical Scavengers ; pharmacology ; therapeutic use ; Male ; Malondialdehyde ; metabolism ; Neuroprotective Agents ; pharmacology ; therapeutic use ; Random Allocation ; Rats ; Rats, Sprague-Dawley ; Spinal Cord Injuries ; drug therapy ; metabolism ; Superoxide Dismutase ; metabolism

OBJECTIVE: To investigate the neuroprotective mechanism of tetrahydroxystilbene glucoside (TSG), a Chinese medicine, on rats after cerebral ischemia-reperfusion. METHODS: A total of 96 Sprague-Dawley male rats were divided into 4 groups (n=24): a control group, an ischemia-reperfusion (I/R) model group, a low dose TSG [60 mg/(kg.d)]group, and a high dose TSG [120 mg/(kg.d)]group. After 6 days intragastric (ig) administration of TSG or natural saline (I/R group), reversible middle cerebral artery occlusion (MCAO) model was established by intraluminal suture technique. The rats of control group were operated on while the middle cerebral artery was not blocked. At 6 h, 24 h, 48 h, and 7 d after the reperfusion, behavior test was used to evaluate the neurological deficiency of each group. The protein expressions of nerve growth factor (NGF), growth associated protein (GAP)-43, and protein kinase A catalytic subunit (PKAc) in the cortex were measured by immunohistochemical method. RESULTS: Compared with the I/R group, the neurological defect scores of the 2 TSG groups were significantly lower except at 6 h after the reperfusion. Compared with the I/R group, the protein expression of NGF, GAP-43, and PKAc after the reperfusion of the 2 TSG groups increased significantly. CONCLUSION The protein expression of NGF may increase when treated with TSG after cerebral ischemia-reperfusion, which activates the PKA pathway and increases the protein expression of GAP-43 that protects the neuron.
Animals ; GAP-43 Protein ; metabolism ; Glucosides ; pharmacology ; therapeutic use ; Infarction, Middle Cerebral Artery ; complications ; drug therapy ; Male ; Nerve Growth Factor ; metabolism ; Neuroprotective Agents ; pharmacology ; therapeutic use ; Random Allocation ; Rats ; Rats, Sprague-Dawley ; Reperfusion Injury ; prevention & control ; Stilbenes ; pharmacology ; therapeutic use

Progress of studies concerning the protective effect of ginsenoside on central nerve system (CNS) in animals and its mechanism published in recent decade were reviewed in this paper. It showed that ginsenosides could improve the learning capacity and memory in normal, aged animals, as well as in model animals with impaired memory. The mechanism of the protective effect on CNS involves the effects on calcium channel blockade, glutamate and gamma-aminobutyric acid, antiperoxidation, estrogen-like action, nitric oxide and its synthase, also the inhibition on cerebral nerve cell apoptosis and amelioration on mitochondrial dysfunction, etc.
Aging ; drug effects ; Animals ; Avoidance Learning ; drug effects ; Ginsenosides ; pharmacology ; Memory ; drug effects ; Memory Disorders ; drug therapy ; Neuroprotective Agents ; pharmacology ; therapeutic use ; Nitric Oxide Synthase ; metabolism