ABSTRACT
Diosgenin, a steroidal sapogenin, obtained from Trigonella foenum-graecum, Dioscorea, and Rhizoma polgonati, has shown high potential and interest in the treatment of various cancers such as oral squamous cell carcinoma, laryngeal cancer, esophageal cancer, liver cancer, gastric cancer, lung cancer, cervical cancer, prostate cancer, glioma, and leukemia. This article aims to provide an overview of the in vivo, in vitro, and clinical studies reporting the diosgenin's anticancer effects. Preclinical studies have shown promising effects of diosgenin on inhibiting tumor cell proliferation and growth, promoting apoptosis, inducing differentiation and autophagy, inhibiting tumor cell metastasis and invasion, blocking cell cycle, regulating immunity and improving gut microbiome. Clinical investigations have revealed clinical dosage and safety property of diosgenin. Furthermore, in order to improve the biological activity and bioavailability of diosgenin, this review focuses on the development of diosgenin nano drug carriers, combined drugs and the diosgenin derivatives. However, further designed trials are needed to unravel the diosgenin's deficiencies in clinical application.
Subject(s)
Carcinoma, Squamous Cell , Diosgenin , Mouth Neoplasms , Prostatic Neoplasms , Male , Humans , Carcinoma, Squamous Cell/drug therapy , Diosgenin/pharmacology , Diosgenin/therapeutic use , Diosgenin/metabolism , Mouth Neoplasms/drug therapy , Apoptosis , Prostatic Neoplasms/drug therapyABSTRACT
The massive adoption of renewable energy especially photovoltaic (PVs) panels is expected to create a huge waste stream once they reach end-of-life (EoL). Despite having the highest embodied energy, present photovoltaic recycling neglects the high purity silicon found in the PV cell. Herein, a scalable and low energy process is developed to recover pristine silicon from EoL solar panel through a method which avoids energy-intensive high temperature processes. The extracted silicon was upcycled to form lithium-ion battery anodes with performances comparable to as-purchased silicon. The anodes retained 87.5 % capacity after 200â cycles while maintaining high coulombic efficiency (>99 %) at 0.5â A g-1 charging rate. This simple and scalable process to upcycle EoL-solar panels into high value silicon-based anodes can narrow the gap towards a net-zero waste economy.
ABSTRACT
Chlorogenic acid (CGA) is a kind of traditional Chinese medicine, abundant in honeysuckle and eucommia, and has a wide range of biological activities, and pharmacological effects. Previous studies have shown that CGA can regulate learning, memory, cognitive ability, coupled with improvement to anxiety, depression, and other post-traumatic stress disorder (PTSD)-like symptoms. This article explores the protective effects of CGA on neurons through its anti-apoptotic effect, inhibition of neuroinflammation and oxidative stress, which may be the mechanisms of its improvement of PTSD-like symptoms. It may provide a new therapeutic strategy for the treatment of PTSD and its comorbidities.
Subject(s)
Stress Disorders, Post-Traumatic , Anxiety , Anxiety Disorders , Chlorogenic Acid/pharmacology , Chlorogenic Acid/therapeutic use , Humans , Neuroinflammatory Diseases , Stress Disorders, Post-Traumatic/drug therapyABSTRACT
Neurological diseases bring great mental and physical torture to the patients, and have long-term and sustained negative effects on families and society. The attention to neurological diseases is increasing, and the improvement of the material level is accompanied by an increase in the demand for mental level. The p75 neurotrophin receptor (p75NTR) is a low-affinity neurotrophin receptor and involved in diverse and pleiotropic effects in the developmental and adult central nervous system (CNS). Since neurological diseases are usually accompanied by the regression of memory, the pathogenesis of p75NTR also activates and inhibits other signaling pathways, which has a serious impact on the learning and memory of patients. The results of studies shown that p75NTR is associated with LTP/LTD-induced synaptic enhancement and inhibition, suggest that p75NTR may be involved in the progression of synaptic plasticity. And its proapoptotic effect is associated with activation of proBDNF and inhibition of proNGF, and TrkA/p75NTR imbalance leads to pro-survival or proapoptotic phenomena. It can be inferred that p75NTR mediates apoptosis in the hippocampus and amygdale, which may affect learning and memory behavior. This article mainly discusses the relationship between p75NTR and learning memory and associated mechanisms, which may provide some new ideas for the treatment of neurological diseases.
Subject(s)
Hippocampus , Receptors, Nerve Growth Factor , Apoptosis , Hippocampus/metabolism , Humans , Nerve Tissue Proteins , Neuronal Plasticity , Receptor, Nerve Growth Factor/metabolism , Receptors, Nerve Growth Factor/metabolism , Signal TransductionABSTRACT
Nogo-66 receptor (NgR) and paired immunoglobulin-like receptor B (PirB) are two common receptors of various myelin-associated inhibitors (MAIs) and, thus, play an important role in MAIs-induced inhibitory signalling of regeneration following spinal cord injury (SCI). Based on the concept of protective autoimmunity, vaccine approaches could induce the production of antibodies against inhibitors in myelin, such as using purified myelin, spinal cord homogenates, or MAIs receptor NgR, in order to block the inhibitory effects and promote functional recovery in SCI models. However, due to the complication of the molecules and the mechanisms involved in MAIs-mediated inhibitory signalling, these immunotherapy strategies have yielded inconsistent outcomes. Therefore, we hypothesized that the choice and modification of self-antigens, and co-regulating multiple targets, may be more effective in repairing the injured spinal cord and improving functional recovery. In this study, NgR and PirB were selected to construct a double-targeted granulocyte-macrophage colony stimulating factor-NgR-PirB (GMCSF-NgR-PirB) nucleic acid vaccine, and investigate the efficacy of this immunotherapy in a spinal cord injury model in rats. The results showed that this vaccination could stimulate the production of antibodies against NgR and PirB, block the inhibitory effects mediated by various MAIs, and promote nerve regeneration and functional recovery after spinal cord injury. These findings suggest that nucleic acid vaccination against NgR and PirB can be a promising therapeutic strategy for SCI and other central nervous system diseases and injuries.
Subject(s)
Immunotherapy/methods , Nerve Regeneration/immunology , Nogo Receptor 1/immunology , Spinal Cord Injuries/therapy , Vaccines, DNA/therapeutic use , Animals , Female , Rats , Rats, Sprague-Dawley , Recovery of Function/immunology , Spinal Cord Injuries/immunology , VaccinationABSTRACT
The studying of synaptic plasticity, the ability of synaptic connections between neurons to be weakened or strengthened and specifically long-term potentiation (LTP) and long-term depression (LTD), is one of the most active areas of research in neuroscience. The process of synaptic connections playing a crucial role in improving cognitive processes is important to the processing of information in brain. In general, the dysfunction of synaptic plasticity was involved in a wide spectrum of central nervous system (CNS) disorders, including some neurodegenerative disorders. Thus, synaptic plasticity which is a dysfunction reported in neurodegenerative disorders may also be involved in posttraumatic stress disorder (PTSD), an anxiety and/or memory disorder developed after experiencing natural disasters, domestic violence or combat-related trauma. In this review, we mainly focus on discussing the biological function and mechanism for diagnostics and therapy of synaptic plasticity in PTSD and associated comorbidities, such as schizophrenia, depression, sleep disturbances and alcohol dependence, and further studying the molecular mechanisms of PTSD with a particular focus on the LTP/LTD, glutamatergic ligand-receptor systems, voltage-gated calcium channels (VGCCs) and brain-derived neurotrophic factor (BDNF)-tyrosine kinase B (TrkB). The summarized function and mechanism of synaptic plasticity in PTSD and its comorbidities may help us further understand PTSD and provide insight into novel neuroplasticity modifying for diagnostics and treatment for PTSD.
Subject(s)
Neuronal Plasticity , Stress Disorders, Post-Traumatic/diagnosis , Stress Disorders, Post-Traumatic/therapy , Animals , Humans , Neuronal Plasticity/drug effects , Neuroprotective Agents/pharmacology , Stress Disorders, Post-Traumatic/complications , Stress Disorders, Post-Traumatic/physiopathologyABSTRACT
High salt intake has been known to cause hypertension and other side effects. However, it is still unclear whether it also affects fibrosis in the mature or developing liver. This study demonstrates that high salt exposure in mice (4% NaCl in drinking water) and chick embryo (calculated final osmolality of the egg was 300 mosm/L) could lead to derangement of the hepatic cords and liver fibrosis using H&E, PAS, Masson, and Sirius red staining. Meanwhile, Desmin immunofluorescent staining of mouse and chick embryo livers indicated that hepatic stellate cells were activated after the high salt exposure. pHIS3 and BrdU immunohistological staining of mouse and chick embryo livers indicated that cell proliferation decreased; as well, TUNEL analyses indicated that cell apoptosis increased in the presence of high salt exposure. Next, dihydroethidium staining on the cultured chick hepatocytes indicated the excess ROS was generated following high salt exposure. Furthermore, AAPH (a known inducer of ROS production) treatment also induced the liver fibrosis in chick embryo. Positive Nrf2 and Keap1 immunohistological staining on mouse liver suggested that Nrf2/Keap1 signaling was involved in high salt induced ROS production. Finally, the CCK8 assay was used to determine whether or not the growth inhibitory effect induced by high salt exposure can be rescued by antioxidant vitamin C. Meanwhile, the RT-PCR result indicated that the Nrf2/Keap1 downsteam genes including HO-1, NQO-1, and SOD2 were involved in this process. In sum, these experiments suggest that high salt intake would lead to high risk of liver damage and fibrosis in both adults and developing embryos. The pathological mechanism may be the result from an imbalance between oxidative stress and the antioxidant system.
Subject(s)
Liver Cirrhosis/metabolism , Reactive Oxygen Species/metabolism , Sodium Chloride/adverse effects , Adaptor Proteins, Signal Transducing/genetics , Adaptor Proteins, Signal Transducing/metabolism , Animals , Apoptosis , Cell Proliferation , Chick Embryo , Cytoskeletal Proteins/genetics , Cytoskeletal Proteins/metabolism , Hepatocytes/cytology , Hepatocytes/metabolism , Humans , Kelch-Like ECH-Associated Protein 1 , Liver Cirrhosis/etiology , Liver Cirrhosis/genetics , Liver Cirrhosis/physiopathology , Male , Mice , Mice, Inbred C57BL , NF-E2-Related Factor 2/genetics , NF-E2-Related Factor 2/metabolism , Oxidative Stress , Sodium Chloride/analysis , Sodium Chloride/metabolismABSTRACT
OBJECTIVE: To study the sedative, hypnotic and antiseizure effects of the compound preparation of gardenia oil and jujube seed oil in mice and investigate the interaction of the two drugs in this preparation. METHODS: The compound preparation was administered intragastrically in mice, whose spontaneous activity was observed along with their tolerance of the preparation after long-term administration. The hypnotic effect of the compound was assessed by investigating the changes in the pentobarbital sodium-induced sleeping. The compound was tested for its antiseizure effect in mice with pentetrazole-induced clonic and tonic convulsion. Diazepam was used as the standard control in all experiments. RESULTS: The jujube seed oil, the gardenia oil and their compound all inhibited spontaneous activities of the mice. Compared with diazepam, the compound showed slow action in producing the sedative effect, which increased gradually with prolonged drug administration without obvious drug tolerance responses. The compound and the two oils all showed synergistic action with pentobarbital sodium in inducing sleeping of the mice. Prescription study showed that the compound produced stronger sedative and hypnotic effects than either of the oils. The two oils and the compound did not show significant antiseizure effects in mice. CONCLUSION: The compound of jujube seed oil and gardenia oil has sedative and hypnotic effects in mice, and the two oils in the compound show obvious synergistic effect.
Subject(s)
Anticonvulsants/pharmacology , Gardenia/chemistry , Hypnotics and Sedatives/pharmacology , Plant Oils/pharmacology , Ziziphus/chemistry , Animals , Drugs, Chinese Herbal/pharmacology , Mice , Mice, Inbred ICR , Seeds/chemistryABSTRACT
In the title compound, C(8)H(11)BrN(+)·Br(-)·H(2)O, a network of N-Hâ¯O, N-Hâ¯Br and O-Hâ¯Br hydrogen bonds helps to consolidate the crystal packing.
ABSTRACT
OBJECTIVE: To observe the effect of Gusongbao (GSB) on proliferation and metabolism of osteoblast cultured in vitro. METHODS: Old rats, aged 18 months, were given GSB 1.5 g/kg, twice a day for 3 days by intragastric perfusion. Blood of the rats was collected 1 hr after the final perfusion to isolate serum for preparing, with D8900 medium, the culture media containing 7.5% or 15% GSB, which was used to culture osteoblast for 24 hrs. Besides, D8900 media containing 7.5% or 15% old rats'serum without medication, containing 20 mumol/L, sodium fluoride, and simple D8900 medium were prepared for control. The cell proliferation was detected by MTT method, and the changes of Ca2+ concentration and ALP content in supernatant of culture were also observed. RESULTS: The osteoblast proliferation cultured in GSB serum containing medium was significantly increased than those cultured in the other control media (P < 0.01), at the same time, the Ca2+ consumption increased and the ALP content elevated significantly (P < 0.05, P < 0.01). CONCLUSION: GSB could promote the DNA synthesis, increase the utilization of Ca2+ and accelerate the growth and proliferation of osteoblast.