The protective effect of erythropoietin and its novel derived peptides in peripheral nerve injury.

Peripheral nerve injury seriously endangers human life and health, but there is no clinical drug for the treatment of peripheral nerve injury, so it is imperative to develop drugs to promote the repair of peripheral nerve injury. Erythropoietin (EPO) not only has the traditional role of promoting erythropoiesis, but also has a tissue-protective effect. Over the past few decades, researchers have confirmed that EPO has neuroprotective effects.

CXCL1-CXCR2 axis mediates inflammatory response after sciatic nerve injury by regulating macrophage infiltration.

Macrophages play a crucial role in the inflammatory response following sciatic nerve injury. Studies have demonstrated that C-X-C motif chemokine (CXCL) 1 recruit macrophages by binding to C-X-C chemokine receptor (CXCR) 2 and participates in the inflammatory response of various diseases. Based on these findings, we aimed to explore the role of the CXCL1-CXCR2 axis in the repair process after peripheral nerve injury.

Pathogenic Th17 cell-mediated liver fibrosis contributes to resistance to PD-L1 antibody immunotherapy in hepatocellular carcinoma.

Understanding the mechanisms of resistance of hepatocellular carcinoma (HCC) to targeted therapies and immune checkpoint blockade is critical for the development of new combination therapies and improving patient survival. Here, we found that in HCC, anti-programmed cell death 1 ligand 1 (PD-L1) therapy reduces liver cancer growth, but the tumors eventually become resistant to continued therapy. Experimental analyses shows that the infiltration of pathogenic T helper 17 (pTh17) cells increases in drug-resistant HCC, and pTh17 cells secrete interleukin-17A (IL-17A), which promotes the expression of PD-L1 on the surface of HCC cells and produces resistance to anti-PD-L1 therapy.

IL-17A functions and the therapeutic use of IL-17A and IL-17RA targeted antibodies for cancer treatment.

Interleukin 17A (IL-17A) is a major member of the IL-17 cytokine family and is produced mainly by T helper 17 (Th17) cells. Other cells such as CD8 T cells, γδ T cells, natural killer T cells and innate lymphoid-like cells can also produce IL-17A. In healthy individuals, IL-17A has a host-protective capacity, but excessive elevation of IL-17A is associated with the development of autoimmune diseases and cancer.

The CXCL12-CXCR4-NLRP3 axis promotes Schwann cell pyroptosis and sciatic nerve demyelination in rats.

Studies have shown that the activation of the NOD-like receptor protein 3 (NLRP3) inflammasome is detrimental to the functional recovery of the sciatic nerve, but the regulatory mechanisms of the NLRP3 inflammasome in peripheral nerves are unclear. C-X-C motif chemokine 12 (CXCL12) can bind to C-X-C chemokine receptor type 4 (CXCR4) and participate in a wide range of nerve inflammation by regulating the NLRP3 inflammasome. Based on these, we explore whether CXCL12-CXCR4 axis regulates the NLRP3 inflammasome in the peripheral nerve.

The role of CXCL1/CXCR2 axis in neurological diseases.

The C-X-C chemokine ligand (CXCL) 1 and its receptor C-X-C chemokine receptor (CXCR) 2 are widely expressed in the peripheral nervous systems (PNS) and central nervous systems (CNS) and are involved in the development of inflammation and pain after various nerve injuries. Once a nerve is damaged, it affects not only the neuron itself but also lesions elsewhere in its dominant site. After the CXCL1/CXCR2 axis is activated, multiple downstream pathways can be activated, such as c-Raf/MAPK/AP-1, p-PKC-μ/p-ILK/NLRP3, JAK2/STAT3, TAK1/NF-κB, etc.

The role of the sex hormone-gut microbiome axis in tumor immunotherapy.

Accumulating evidence suggested that both gut microbiome and sex play a critical role in the efficacy of immune checkpoint blockade therapy. Considering the reciprocal relationship between sex hormones and gut microbiome, the sex hormone-gut microbiome axis may participate in the regulation of the response to immune checkpoint inhibitors (ICIs). In this review, it was attempted to summarize the current knowledge about the influences of both sex and gut microbiome on the antitumor efficacy of ICIs and describe the interaction between sex hormones and gut microbiome.

Research progress of targeting NLRP3 inflammasome in peripheral nerve injury and pain.

Nerve injury and nerve pain are common diseases caused by neuroinflammation. Numerous studies have shown that the activation of NLRP3 (nod-like receptor family, pyrin domain-containing 3) inflammasome is involved in a various inflammatory response, such as Alzheimer's disease, diabetes, nerve damage and other diseases. The NLRP3 inflammasome is a complex containing NLRP3 protein, ASC (apoptosis-associated speckle-like protein), and pro-caspase-1, which is highly expressed and activated to promote the secretion of IL-1β and IL-18 in response to the stimulation of danger-associated molecular patterns (DAMPs) and pathogen-associated molecular patterns (PAMPs) in immune cells such as macrophages and dendritic cells.

Identification of Metabolites and Metabolic Pathways Related to Treatment with Bufei Yishen Formula in a Rat COPD Model Using HPLC Q-TOF/MS.

As a traditional Chinese medicine, Bufei Yishen Formula (BYF) is widely used in China as an effective treatment for chronic obstructive pulmonary disease (COPD). Because of the component complexity and multiple activities of Chinese herbs, the mechanism whereby BYF affects COPD is not yet fully understood. Herein, pulmonary function experiments and histomorphological assessments were used to evaluate the curative effect of BYF, which showed that BYF had an effect on COPD.

Metabolomics study on model rats of chronic obstructive pulmonary disease treated with Bu‑Fei Jian‑Pi.

The therapeutic effect of Traditional Chinese Medicine (TCM) on chronic obstructive pulmonary disease (COPD) has been know for numerous years; however, the mechanism of action of the beneficial effects of TCM remains to be elucidated. The present study aimed to investigate the molecular mechanisms of COPD through metabolomic analysis as well as explore the targets and intervention mechanisms of TCM therapy using the common TCM granules Bu‑Fei Jian‑Pi. COPD rat models were established using smoke inhalations and recurrent bacterial infections.

Effects and mechanism of bufei yishen formula in a rat chronic obstructive pulmonary disease model.

Bufei Yishen Formula (BYF) has been used for centuries in Asia to effectively treat patients with chronic obstructive pulmonary disease (COPD). This study established a COPD animal model in rats, wherein three groups (control, COPD, and BYF) were used to evaluate the mechanism(s) and curative effect of BYF. Pulmonary function and histomorphology demonstrated that BYF had an evident effect on COPD.

Intravenous dezocine pretreatment reduces the incidence and intensity of myoclonus induced by etomidate.

To evaluate the suppressive effect of intravenous dezocine on the incidence and severity of myoclonic movements induced by etomidate, a total of 80 patients, American Society of Anesthesiologists physical status I-II, were randomized into two equally sized groups (n = 40). These two groups were assigned to give either intravenous dezocine 0.1 mg/kg or a matching placebo (equal volume of 0.

Long-term effects of three Tiao-Bu Fei-Shen therapies on NF-κB/TGF-β1/smad2 signaling in rats with chronic obstructive pulmonary disease.

Background: The three Tiao-Bu Fei-Shen (Bufei Jianpi, Bufei Yishen, Yiqi Zishen) granules have been confirmed for their beneficial clinical efficacy in chronic obstructive pulmonary disease (COPD) patients on reducing frequency and duration of acute exacerbation, improving syndromes, pulmonary function and exercise capacity. But the short- or long-term mechanism of them is not fully clear. Nuclear factor (NF)-κB/transforming growth factor (TGF)-β1/smad2 signaling pathway is involved in the progress of inflammation and remodeling in chronic obstructive pulmonary disease COPD.

[Influence and long-term effects of three methods for regulating and invigorating fei-shen on T lymphocyte subsets and CD4+ CD25+ in COPD rats].

Objective: To evaluate the therapeutic and long-term effects of three methods for regulating and invigorating Fei-Shen [reinforcing Fei and invigorating Pi (RFIP), reinforcing Fei and invigorating Shen (RFIS), benefiting qi and nourishing Shen (BQNS)] on T lymphocyte subsets and CD4+ CD25+ in rats with chronic obstructive pulmonary disease (COPD).

Methods: Totally 120 rats were randomly divided into the control group, the model group, the RFIP group, the RFIS group, the BQNS group, and the aminophylline group, 20 in each group. Except those in the control group, the rest rats were exposed to cigarette smoking and bacterial infection to prepare the COPD rat model.

[Impact and long-term effect of three prescriptions regulating and tonifying lung and kidney on JAK/STAT signaling in rats].

Objective: To evaluate the impact and long-term effect of three prescriptions regulating and tonifying lung and kidney (prescription tonifying lung and spleen, prescription tonifying lung and kidney, and prescription tonifying Qi and kidney) on JAK/STAT signaling of COPD rats.

Method: Rats were randomly divided into the control group, the model group, the Bufeijianpi group, the Bufeiyishen group, the Yiqizishen group and the aminophyline group. The COPD rat model was established by smoke inhalations and bacterial infections.

Long-term effects of Tiaobu Feishen therapies on systemic and local inflammation responses in rats with stable chronic obstructive pulmonary disease.

Objective: To evaluate the influence and long-term effects on systemic and local inflammation responses in rat with stable chronic obstructive pulmonary disease (COPD) treated with traditional Chinese medicine (TCM) for regulating and invigorating the lung and kidney, including invigorating the lung and spleen (Bufei Jianpi) therapy, supplementing the lung and kidney (Bufei Yishen) therapy, and nourishing qi and kidney (Yiqi Zishen) therapy.

Methods: Rats were randomly divided into six groups: control, model, aminophyline, Bufei Jianpi, Bufei Yishen and Yiqi Zishen groups. The stable COPD model of rat was duplicated by cigarette smoke inhalations and bacterial infection.

A rat model for stable chronic obstructive pulmonary disease induced by cigarette smoke inhalation and repetitive bacterial infection.

To develop a stable chronic obstructive pulmonary disease (COPD) model in rats. Sprague-Dawley rats were treated with cigarette-smoke inhalation (CSI) for 12 weeks, repetitive bacterial infection (RBI) for 8 weeks, or the combination of the two (CCR) for 12 weeks and followed up for the additional 20 weeks. Tidal volume (V(T)), peak expiratory flow (PEF) and 50% V(T) expiratory flow (EF(50)), histological changes in the lungs, and levels of the cytokines tumor necrosis factor (TNF)-α, interleukin (IL)-8, and IL-10 in serum and bronchial alveolar lavage fluid (BALF) were examined at intervals during the 32 week study period.