Carbon-based inorganic CsPbX3 (X = I, Br, Cl) perovskite solar cells (PSCs) are attracting great attention in the photovoltaic field because of their low cost, simple process, and superior thermal stability. However, the large difference in energy band between the CsPbX3 and carbon electrode leads to the poor hole extraction and unfavorable charge recombination, thus deteriorating device’s efficiency. In this work, a solution-processed dopant-free tin phthalocyanine (SnPc) film is used as a hole-transport layer (HTL) to fabricate carbon-based CsPbI2Br PSCs by a low-temperature process. At the optimal process, the device achieves a maximum efficiency of 11.39% with less hysteresis, which is much higher than 9.22% of reference device without the SnPc HTL. Moreover, the unencapsulated device exhibits the improved stability and remains about 90% of its initial efficiency after 30 days in ambient air (20–25 °C) with 25–35% relative humidity (RH). This finding reveals that the solution-processed dopant-free SnPc HTL can significantly promote charge transport and suppress charge recombination at the CsPbI2Br/carbon interface. This work provides a low-temperature and solution-processed method to fabricate the efficient and stable carbon-based inorganic PSCs.
Exposure to carbon disulfide (CS 2 ) has been associated with an increased incidence of parkinsonism in workers, but the mechanism underlying this association remains unclear. Using a rat model, we investigated the effects of chronic CS 2 exposure on parkinsonian pathology. Our results showed that CS 2 exposure leads to significant motor impairment and neuronal damage, including loss of dopaminergic neurons and degeneration of the substantia nigra pars compacta (SNpc). The immunoassays revealed that exposure to CS 2 induces aggregation of α-synuclein and phosphorylated α-synuclein, as well as activation of necroptosis in the SNpc. Furthermore, in vitro and in vivo experiments demonstrated that the interaction between α-synuclein and the necrosome complex (RIP1, RIP3, and MLKL) is responsible for the loss of neuronal cells after CS 2 exposure. Taken together, our results demonstrate that CS 2 -mediated α-synuclein aggregation can induce dopaminergic neuron damage and parkinsonian behavior through interaction with the necrosome complex.
Salidroside, a phenylpropanoid glycoside, is the main bioactive component of Rhodiola rosea L. Salidroside has prominent anti-stroke effects in cerebral ischemia/reperfusion models. However, the underlying mechanisms of its actions are poorly understood. This study examined the anti-stroke effects of salidroside in middle cerebral artery occlusion (MCAO)-induced rat model of stroke and its potential mechanisms involving the dopaminergic system. Salidroside administration increased the levels of dopamine (DA), homovanillic acid (HVA), and 3,4-dihydroxyphenylacetic acid (DOPAC) in the ipsilateral striatum after induction of transient ischemia, which were assessed using microdialysis with high-performance liquid chromatography coupled with electrochemical detection (HPLC-ECD). Furthermore, treatment with salidroside ameliorated neurobehavioral impairment, assessed with the modified neurological severity scores (mNSS), the balance beam test, and the foot fault test. Moreover, enzyme-linked immunosorbent assay (ELISA) suggested that MCAO-induced reduction in monoamine oxidase (MAO) was inhibited by salidroside. Immunohistochemical and immunofluorescence analyses revealed high level of tyrosine hydroxylase (TH) in the ipsilateral striatal caudate putamen (CPu) after cerebral ischemia/reperfusion, which could be further elevated by salidroside. In addition, salidroside could reverse the decreased immunoreactivity of TH in the substantia nigra pars compacta (SNpc). These results suggest that the anti-stroke effects of salidroside in MCAO-induced cerebral ischemia/reperfusion may involve the modulation of monoamine metabolism in the striatum and SNpc, which may be related to the function of the dopaminergic system in the rat brain.
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