Protective effect of liquiritin against cisplatin-induced liver injury in mice through reduction of inflammation, oxidative stress, apoptosis and inhibition of p38 MAPK/p53 pathway based on network pharmacology and in experimental validation.

Ethnopharmacological Relevance: Cisplatin is widely used in chemotherapy, but hepatotoxicity limits its effectiveness. Liquiritin has liver-protective effects, but its mechanisms have not been elucidated in combination with cisplatin for liver-injury treatment in mice.

Aim Of The Study: This investigation explored liquiritin's protective effect against cisplatin-induced liver damage in mice and its mechanisms.

A synthetic peptide, derived from neurotoxin GsMTx4, acts as a non-opioid analgesic to alleviate mechanical and neuropathic pain through the TRPV4 channel.

Mechanical pain is one of the most common causes of clinical pain, but there remains a lack of effective treatment for debilitating mechanical and chronic forms of neuropathic pain. Recently, neurotoxin GsMTx4, a selective mechanosensitive (MS) channel inhibitor, has been found to be effective, while the underlying mechanism remains elusive. Here, with multiple rodent pain models, we demonstrated that a GsMTx4-based 17-residue peptide, which we call P10581, was able to reduce mechanical hyperalgesia and neuropathic pain.

The mechanism of Ca-independent activation of BKCa channels in mouse inner hair cells and the crucial role of the BK channels in auditory perception.

BK channels are expressed in mouse cochlear inner hair cells (IHCs) and exhibit Ca-independent activation at negative potentials. However, the mechanism underlying Ca-independent activation of the BK channels in mouse IHCs remains unknown. In this study, we found the BK channel expressed in IHCs contains both the stress-axis regulated exon 2 variant and an alternative splice of exon9 (alt9), which significantly shift the voltage dependence of the BK channels when coexpressed with LRRC52 in 0 [Ca].

What is behind the meta-learning initialization of adaptive filter? - A naive method for accelerating convergence of adaptive multichannel active noise control.

Active noise control (ANC) is a typical signal-processing technique that has recently been utilized extensively to combat the urban noise problem. Although numerous advanced adaptive algorithms have been devised to enhance noise reduction performance, few of them have been implemented in actual ANC products due to their high computational complexity and slow convergence. With the rapid development of deep learning technology, Meta-learning-based initialization appears to become an efficient and cost-effective method for accelerating the convergence of adaptive algorithms.

Downregulating miR-184 relieves calcium oxalate crystal-mediated renal cell damage via activating the Rap1 signaling pathway.

Background: Renal calculi are a very prevalent disease with a high incidence. Calcium oxalate (CaOx) is a primary constituent of kidney stones. Our paper probes the regulatory function and mechanism of miR-184 in CaOx-mediated renal cell damage.

μ opioid receptor carboxyl terminal-derived peptide alleviates morphine tolerance by inhibiting β-arrestin2.

The interaction between the μ opioid receptor (MOR) and β-arrestin2 serves as a model for addressing morphine tolerance. A peptide was designed to alleviate morphine tolerance through interfering with the interaction of MOR and β-arrestin2. We developed a peptide derived from MOR.

Identification of the Acid-Sensitive Site Critical for Chloral Hydrate (CH) Activation of the Proton-Activated Chloride Channel.

The transmembrane protein TMEM206 was recently identified as the molecular basis of the extracellular proton-activated Cl channel (PAC), which plays an essential role in neuronal death in ischemia-reperfusion. The PAC channel is activated by extracellular acid, but the proton-sensitive mechanism remains unclear, although different acid-sensitive pockets have been suggested based on the cryo-EM structure of the human PAC (hPAC) channel. In the present study, we firstly identified two acidic amino acid residues that removed the pH-dependent activation of the hPAC channel by neutralization all the conservative negative charged residues located in the extracellular domain of the hPAC channel and some positively charged residues at the hotspot combined with two-electrode voltage-clamp (TEVC) recording in the oocytes system.

Construction of a highly error-prone DNA polymerase for developing organelle mutation systems.

A novel family of DNA polymerases replicates organelle genomes in a wide distribution of taxa encompassing plants and protozoans. Making error-prone mutator versions of gamma DNA polymerases revolutionised our understanding of animal mitochondrial genomes but similar advances have not been made for the organelle DNA polymerases present in plant mitochondria and chloroplasts. We tested the fidelities of error prone tobacco organelle DNA polymerases using a novel positive selection method involving replication of the phage lambda cI repressor gene.

C/EBPα Regulates FOXC1 to Modulate Tumor Growth by Interacting with PPARγ in Hepatocellular Carcinoma.

Background: Forkhead box C1 (FOXC1) is an important cancer-associated gene in tumor. PPAR-γ and C/EBPα are both transcriptional regulators involved in tumor development.

Objective: We aimed to clarify the function of PPAR-γ, C/EBPα in hepatocellular carcinoma (HCC) and the relationship of PPAR-γ, C/EBPα and FOXC1 in HCC.

Emodin, a natural anthraquinone, suppresses liver cancer in vitro and in vivo by regulating VEGFR and miR-34a.

The pharmacokinetic (PK) and potential effects of Emodin on liver cancer were systematically evaluated in this study. Both the intragastric administration (i.g.

Necrostatin-1 inhibits the degeneration of neural cells induced by aluminum exposure.

Purpose: There are many in vivo and in vitro studies suggested the involvement of apoptosis in neurodegenerative processes. There is considerable evidence that various complex events may contribute to neural cell death. The present study focuses on the underlined neurodegenerative mechanism and the preventive effect of necrostatin-1 (Nec-1) on neural cell death induced by aluminum (Al).

[Changes of brain oxidative stress induced by nano-alumina in ICR mice].

Objective: To investigate the brain oxidative stress injury induced by nano-alumina particles in ICR mice.

Methods: Sixty male ICR mice were randomly divided into 6 groups: control group, solvent control group, 100 mg/kg micro-alumina particles group, 3 groups exposed to nano-alumina particles at the doses of 50, 100 and 200 mg/kg. The mice were exposed by nasal drip for 30 days.