Co-treatment of betulin and gefitinib is effective against EGFR wild-type/KRAS-mutant non-small cell lung cancer by inducing ferroptosis.

Clinical trials suggest that non-small-cell lung cancer (NSCLC) patients with KRAS mutations and wild-type EGFR have reduced benefits from gefitinib treatment. Ferroptosis is a new form of cell death that plays an important role in mediating the sensitivity of EGFR-TIKs. Here, we explored the antitumor ability of gefitinib in combination with betulin to overcome drug resistance through ferroptosis in wild-type EGFR/KRAS-mutant NSCLC cells.

[Effects of L-carnitine on autophagy and apoptosis of mouse pulmonary microvascular endothelial cells induced by lipopolysaccharide].

To investigate the protective effects of L-carnitine (LC) on lipopolysaccharide (LPS) - injured mouse pulmonary microvascular endothelial cells (PMVECs) and its effects on autophagy and apoptosis. Cultured mouse PMVECs were divided into three groups: ① Control group, ② LPS group (10 μg/ml, 3, 6, 12, 24 h), ③ LPS (10 μg/ml, 24 h)+LC (2.5, 5.

[Changes of FLI-1 protein expression in mice with pulmonary endothelial barrier dysfunction following acute lung injury induced by lipopolysaccharide].

To observe changes of Friend leukemia virus integration 1 (FLI-1) protein expression of pulmonary tissue in mice with pulmonary endothelial barrier dysfunction following acute lung injury (ALI) induced by lipopolysaccharide (LPS). The mouse model of ALI was established by injection of LPS (7.5 mg/kg, i.

YAP activity protects against endotoxemic acute lung injury by activating multiple mechanisms.

The roles of the Hippo‑Yes‑associated protein (YAP) pathway in lung injury and repair remain elusive. The present study examined the effects of systemic inhibition or stimulation of YAP activity on lung injury, repair and inflammation in a mouse model of lipopolysaccharide (LPS)‑induced lung injury. Mice were treated with or without YAP inhibitor, verteporfin, or with or without YAP stimulator, XMU‑MP‑1, and intraperitoneally injected with LPS (7.

[Effects of apolipoprotein E on proliferation of mouse pulmonary arterial smooth muscle cells induced by hypoxia].

Objective: To investigate the effects of apolipoprotein E (apoE) on the proliferation of pulmonary arterial smooth muscle cells (PASMCs) induced by hypoxia.

Methods: Primary culture of mouse PASMCs was prepared from male C57BL/6 mouse pulmonary artery by the method of tissue block anchorage. PASMCs were divided into four groups: normoxia group, normoxia with apoE administration group, hypoxia group and hypoxia with apoE administration group.

SIRT1 activation attenuates cardiac fibrosis by endothelial-to-mesenchymal transition.

Endothelial-to-mesenchymal transition (EndMT) is closely related to the pathogenesis of various diseases, including cardiac fibrosis. Transforming growth factor (TGF)-β1 strongly induces EndMT, and sirtuin 1 (SIRT1) may play vital roles in TGF-β/Smad pathway inhibition. This study aimed to determine whether SIRT1 activation inhibits EndMT, thereby attenuating cardiac fibrosis.

[Changes of apoE protein expression in lung of mice with hypoxic pulmonary arterial hypertension].

Objective: To observe the changes of apolipoprotein E (apoE) protein expression of pulmonary tissue in mice with pulmonary hypertension induced by hypoxia.

Methods: The animal model of hypoxic pulmonary hypertension was established by exposing the mice to isobaric hypoxic chamber for 3 weeks (23 h/d, regular chow feed).Twenty male wild type (WT) C57BL/6 mice and twenty apoE gene knockout (apoE-KO) mice were randomly divided into normoxia group and hypoxia group.

[Apelin attenuates hypoxia induced pulmonary hypertension of mice through regulation of lipid metabolism].

Objective: To observe the role of apelin in the prevention of pulmonary hypertension induced by hypoxia in mice.

Methods: Adult male apoE gene knockout (apoE-KO) mice were exposed to isobaric hypoxic chamber (9%~11% O, regular chow feed, 23 h/d)for 3 weeks to establish hypoxia-induced pulmonary hypertension. Thirty apoE-KO mice were randomly divided into normoxia group, hypoxia group and hypoxic with apelin (10 nmol/(kg·d), ip) group.

[Effect of autophagy inhibitor chloroquine on acute alcoholinduced liver disease].

Objectives: To investigate the role of autophagy inhibitor chloroquine (CQ) in acute ethanol-induced liver injury and its mechenism.

Methods: Twenty-one C57BL/6 male mice were randomly divided into three groups:control group, ethanol group, CQ + ethanol group (=7). Mice in ethanol group were administered 33% (v/v) ethanol at a dose of 4.

Effects of curcumin on sodium currents of dorsal root ganglion neurons in type 2 diabetic neuropathic pain rats.

Along with the development of economy and society, type 2 diabetic mellitus (T2DM) has become one of the most common diseases at the global level. As one of the complications of T2DM, diabetic neuropathic pain (DNP) stubbornly and chronically affects the health and life of human beings. In the pain field, dorsal root ganglion (DRG) is generally considered as the first stage of the sensory pathway where the hyperexcitability of injured neurons is associated with different kinds of peripheral neuropathic pains.

[Changes of lipid levels in mice with hypoxic pulmonary arterial hypertension].

Objective: To observe the changes of lipid levels in mice with pulmonary hypertension induced by hypoxia.

Methods: The animal model of hypoxic pulmonary hypertension was established by exposing the mice to isobaric hypoxic chamberfor 3 weeks (23 h/d, regular chow feed). Twenty male C57BL/6 mice were randomlydivided into normoxia group and hypoxia group (=10).

[Role of catestatin in 2K1C-induced renal hypertension in rats and the underlying mechanism].

Objective: To investigate the roles of catestatin (CST) in 2-kidney-1 clip (2K1C)-induced renal hypertension in rats, and to explore the underlying mechanism.

Methods: Thirty six male SD rats were randomly divided into Sham group (=15) and Model group(=21).The model group was performed by 2K1C operation.

Effects of curcumin on TTX-R sodium currents of dorsal root ganglion neurons in type 2 diabetic rats with diabetic neuropathic pain.

Type 2 diabetic mellitus (T2DM) has reached pandemic status and shows no signs of abatement. Diabetic neuropathic pain (DNP) is generally considered to be one of the most common complications of T2DM, which is also recognized as one of the most difficult types of pain to treat. As one kind of peripheral neuropathic pain, DNP manifests typical chronic neuralgia symptoms, including hyperalgesia, allodynia, autotomy, and so on.

LPS Down-Regulates Specificity Protein 1 Activity by Activating NF-κB Pathway in Endotoxemic Mice.

Background: Specificity protein (Sp) 1 mediates the transcription of a large number of constitutive genes encoding physiological mediators. NF-κB mediates the expression of hundreds of inducible genes encoding pathological mediators. Crosstalk between Sp1 and NF-κB pathways could be pathophysiologically significant, but has not been studied.

The Apelin-APJ axis is an endogenous counterinjury mechanism in experimental acute lung injury.

Background: Although the mechanisms and pathways mediating ARDS have been studied extensively, less attention has been given to the mechanisms and pathways that counteract injury responses. This study found that the apelin-APJ pathway is an endogenous counterinjury mechanism that protects against ARDS.

Methods: Using a rat model of oleic acid (OA)-induced ARDS, the effects of ARDS on apelin and APJ receptor expressions and on APJ receptor binding capacity were examined.

Electroacupuncture and A-317491 depress the transmission of pain on primary afferent mediated by the P2X3 receptor in rats with chronic neuropathic pain states.

P2X is a family of ligand-gated ion channels that act through adenosine ATP. The P2X3 receptor plays a key role in the transmission of neuropathic pain at peripheral and spinal sites. Electroacupuncture (EA) has been used to treat neuropathic pain effectively.

[Effect of autophagy inhibitor chloroquine on the proliferation of PASMCs induced by hypoxia].

Objective: To investigate the role of autophagy inhibitor chloroquine (CQ) in the proliferation of pulmonary arterial smooth muscle cells (PASMCs) in hypoxia conditions.

Methods: The following groups in this study were set up: control group, hypoxia group, 50 micromol/L CQ + hypoxia group, 50 micromol/L CQ group. The viability of PASMCs in every group was detected by MTT assay.

[Changes of apelin and its receptor in lung tissue of rats with pulmonary hypertension induced by monocrotaline].

Objective: To observe the change of apelin and its receptor (APJ) in the lung tissue of rats with pulmonary hypertension induced by monocrotaline and to explore its significance.

Methods: Twenty-five male SD rats were randomly divided into control group (n = 10) and monocrotaline group (n = 15). On the twenty-first day after the rats were intraperitoneally injected 60 mg/kg monocrotaline for monocrotaline group or equal volume vehicle for control group, the mean pulmonary artery pressure was measured by right heart catheterization.

Intermedin modulates hypoxic pulmonary vascular remodeling by inhibiting pulmonary artery smooth muscle cell proliferation.

Background: Hypoxic pulmonary arterial hypertension (PAH) is a disabling disease with limited treatment options. Hypoxic pulmonary vascular remodeling is a major cause of hypoxic PAH. Pharmacological agents that can inhibit the remodeling process may have great therapeutic value.

[Migratory properties of vascular smooth muscle cells on extracellular matrix: a study on inverted coverslip migration assay].

Migration of vascular smooth muscle cells (VSMCs) is involved in vascular development and various vascular diseases; however, the molecular mechanisms of VSMC migration remain unclear. In this study, we established an inverted coverslip migration assay to study the migratory properties of cultured VSMCs on extracellular matrix. Pulmonary arterial smooth muscle cells (PASMCs) from rats were cultured and identified by immunocytochemistry.

Effect of safflower injection on endoplasmic reticulum stress-induced apoptosts in rats with hypoxic pulmonary hypertension.

Objective: To explore the effects of safflower injection on prevention and treatment of hypoxic pulmonary hypertension and clarify the function of the endoplasmic reticulum stress apoptosis pathway during the process.

Methods: Thirty male SD rats were randomly grouped as normal control group, hypoxia-hypercapnia group and hypoxia+safflower group. The latter two groups were put in the cabin with oxygen concentration ranged from 9% to 11% and carbon dioxide concentration from 5% to 6%.

[Effect of swimming exercise on the expression of apelin and its receptor in pulmonary tissues of rats with hypoxic pulmonary hypertension].

Objective: To study the effects of swimming exercise on the expression of apelin and its receptor (APJ) system in pulmonary tissues of rats with pulmonary hypertension induced by hypoxia.

Methods: Forty-five male SD rats were randomly divided into control group, hypoxia group (seven-week) and swimming group (four-week swimming group after three-week hypoxia). The animal model of hypoxic pulmonary hypertension was established by exposing the rats to isobaric hypoxic chamber (8 h/d, 6 d/w).

[The time order of autophagy and apoptosis process in the oxidative injury in glioma U251 cells].

Objective: To investigate the time order of autophagy and apoptosis in human U251 cells injury after H2O2 treatment.

Methods: 4 groups in this study were set up, normal control group, 1 mmol/L H2O2 (6 h,12 h, 24 h) group. The viability of U251 cells treated with H2O2 was measured by MTT assay.

[Inhibition of Beclin 1 enhances apoptosis by H2O2 in glioma U251 cells].

Oxidative stress could induce apoptosis and autophagy process simultaneously, but the role of autophagy is still not clear. Beclin 1, a key gene regulating the preautophagosome formation, is involved in the injury induced by oxidative stress. To observe the role of autophagy in H2O2-induced injury of U251 cells, the recombinant plasmid Psilencer3.