Cardiac myxoma (CM) is a prevalent primary cardiac tumor. miR-217 plays a vital role in tumorigenesis of various cancers, however, its role and underlying molecular mechanism in human CM remain poorly understood. Here, we reported that the expression of miR-217 was downregulated in CM tissues and inversely correlated with the expression of Interleukin-6 (IL-6) mRNA. Gain-of-function analysis indicated that overexpression of miR-217 inhibited the proliferation and promoted the apoptosis of the primary CM cells. Bioinformatics analysis showed that IL-6 was a direct target gene of miR-217, which is confirmed by the dual luciferase assays. Moreover, downregulation of IL-6 by small interference RNA (siRNA) mimicked the tumor-suppressive effects of miR-217 in CM. Furthermore, rescue experiments pointed out that restoration of IL-6 expression abrogated the anti-proliferative and pro-apoptotic effect induced by miR-217 overexpression in CM cells. Taken together, we validated that miR-217 could act as a tumor suppressor in CM by directly targeting 3'UTR of IL-6 gene, indicating that manipulation of miR-217 may be a potential therapeutic strategy for CM patients.

Interleukin-6 (IL-6) was proposed to be associated with the severity of coronavirus disease 2019 (COVID-19). The present study aimed to explore the kinetics of IL-6 levels, validate this association in COVID-19 patients, and report preliminary data on the efficacy of IL-6 receptor blockade.

Inflammatory response has been reported to contribute to the renal lesions in rat Thy-1 nephritis (Thy-1N) as an animal model of human mesangioproliferative glomerulonephritis (MsPGN). Besides C5b-9 complex, C5a is also a potent pro-inflammatory mediator and correlated to severity of various nephritic diseases. However, the role of C5a in mediating pro-inflammatory cytokine production in rats with Thy-1N is poorly defined. In the present studies, the levels of C5a, interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) were first determined in the renal tissues of rats with Thy-1N. Then, the expression of IL-6 and TNF-α was detected in rat glomerular mesangial cells (GMC) stimulated with our recombinant rat C5a in vitro. Subsequently, the activation of mitogen-activated protein kinase (MAPK) signaling pathways (p38 MAPK, ERK1/2 and JNK) and their roles in the regulation of IL-6 and TNF-α production were examined in the GMC induced by C5a. The results showed that the levels of C5a, IL-6 and TNF-α were markedly increased in the renal tissues of Thy-1N rats. Rat C5a stimulation in vitro could up-regulate the expression of IL-6 and TNF-α in rat GMC, and the activation of MAPK signaling pathways was involved in the induction of IL-6 and TNF-α. Mechanically, p38 MAPK activation promoted IL-6 production, while either ERK1/2 or JNK activation promoted TNF-α production in the GMC with exposure to C5a. Taken together, these data implicate that C5a induces the synthesis of IL-6 and TNF-α in rat GMC through the activation of MAPK signaling pathways.

Interleukin-6 (IL-6) overproduction has been considered to contribute to inflammatory damage of glomerular mesangial cells (GMCs) in human mesangial proliferative glomerulonephritis (MsPGN) and its rat model called Thy-1 nephritis (Thy-1N). However, the regulatory mechanisms of IL-6 expression in GMCs upon sublytic C5b-9 timulation remain poorly understood. We found that Krüppel-like factor 4 (KLF4) bound to the IL-6 promoter (-618 to -126 nt) and activated IL-6 gene transcription. Furthermore, lysine residue 224 of KLF4 was acetylated by p300/CBP-associated factor (PCAF), which was important for KLF4-mediated transactivation. Moreover, lysine residue 5 on histone H2B and lysine residue 9 on histone H3 at the IL-6 promoter were also acetylated by PCAF, which resulted in an increase in IL-6 transcription. Besides, NF-κB activation promoted IL-6 expression by elevating the expression of PCAF. Overall, these findings suggest that sublytic C5b-9-induced the expression of IL-6 involves KLF4-mediated transactivation, PCAF-mediated acetylation of KLF4 and histones, and NF-κB activation in GMCs.

Chronic obstructive pulmonary disease (COPD) is characterized by the abnormal and chronic lung inflammation. We hypothesized that lung fibroblasts could contribute to the local inflammation and investigated whether low dose theophylline had a beneficial effect on fibroblasts inflammation. Subjects undergoing lobectomy for bronchial carcinoma were enrolled and divided into COPD and control groups according to spirometry. Primary human lung fibroblasts were cultured from peripheral lung tissue distant to tumor tissue. There was a significant increase in both the mRNA expressions and protein levels for IL-6 and IL-8 in fibroblasts in COPD group, and the values were negatively correlated with lung function (P < 0.05). For COPD fibroblasts, the protein levels of IL-6 and IL-8 decreased from 993.0 ± 738.9 pg/mL to 650.1 ± 421.9 pg/mL (P = 0.014) and from 703.1 ± 278.0 pg/mL to 492.0 ± 214.9 pg/mL (P = 0.001), respectively, with 5 μg/mL theophylline treatment. In addition, theophylline at the dose of 5 μg/mL reduced the increased production of IL-6 and IL-8 induced by 1 μg/mL LPS in primary human lung fibroblasts. Our data suggest that lung fibroblasts participate in the chronic inflammation in COPD by releasing IL-6 and IL-8, and low dose theophylline can alleviate the proinflammatory mediators' production by fibroblasts.

As the pandemic progresses, the pathophysiology of COVID-19 is becoming more apparent, and the potential for tocilizumab is increasing. However, the clinical efficacy and safety of tocilizumab in the treatment of COVID-19 patients remain unclear.

Although 9.4 T magnetic resonance imaging (MRI) has been tested in healthy volunteers, its safety in diabetic patients is unclear. Furthermore, the effects of high static magnetic fields (SMFs), especially gradient vs. uniform fields, have not been investigated in diabetics. Here, we investigated the consequences of exposure to 1.0-9.4 T high SMFs of different gradients (>10 T/m vs. 0-10 T/m) on type 1 diabetic (T1D) and type 2 diabetic (T2D) mice. We found that 14 h of prolonged treatment of gradient (as high as 55.5 T/m) high SMFs (1.0-8.6 T) had negative effects on T1D and T2D mice, including spleen, hepatic, and renal tissue impairment and elevated glycosylated serum protein, blood glucose, inflammation, and anxiety, while 9.4 T quasi-uniform SMFs at 0-10 T/m did not induce the same effects. In regular T1D mice (blood glucose ≥16.7 mmol/L), the >10 T/m gradient high SMFs increased malondialdehyde ( P<0.01) and decreased superoxide dismutase ( P<0.05). However, in the severe T1D mice (blood glucose ≥30.0 mmol/L), the >10 T/m gradient high SMFs significantly increased tissue damage and reduced survival rate. In vitro cellular studies showed that gradient high SMFs increased cellular reactive oxygen species and apoptosis and reduced MS-1 cell number and proliferation. Therefore, this study showed that prolonged exposure to high-field (1.0-8.6 T) >10 T/m gradient SMFs (35-1 380 times higher than that of current clinical MRI) can have negative effects on diabetic mice, especially mice with severe T1D, whereas 9.4 T high SMFs at 0-10 T/m did not produce the same effects, providing important information for the future development and clinical application of SMFs, especially high-field MRI.

Response gene to complement (RGC)-32 regulates the cell cycle in response to complement activation. The present study demonstrated that the expression level of RGC-32 is higher in human non-small-cell lung cancer (NSCLC) tissues compared with health controls. Overexpressing RGC-32 induced p65 nucleus translocation, significantly increased nuclear p65 levels and promoted the proliferation of A549 cells. Knockdown of RGC-32 by short hairpin RNA decreased the expression level of nuclear p65 and inhibited cell proliferation. The increase in cell proliferation induced by RGC32 could be abolished by the NF-κB inhibitor pyrrolidine dithiocarbamate. Mechanistic studies indicated that RGC32 mediated NF-κB downstream genes, including vascular cell adhesion protein 1, interleukin-6, cyclin dependent kinase inhibitor 2C, testin and vascular endothelial growth factor A. In summary, the present study demonstrated a novel role of RGC-32 in the progression of NSCLC via the NF-κB pathway and p65. Therefore, RGC-32 could be a potential therapeutic target for NSCLC.

Janus kinase (JAK) 2 plays a pivotal role in the tumorigenesis of signal transducers and activators of transcription (STAT) 3 constitutively activated solid tumors. JAK2 mutations are involved in the pathogenesis of various types of hematopoietic disorders, such as myeloproliferative disorders, polycythemia vera, essential thrombocythemia, and primary myelofibrosis. Thus, small-molecular inhibitors targeting JAK2 are potent for therapy of these diseases. In this study, we screened 1,062,608 drug-like molecules from the ZINC database and 2080 natural product chemicals. We identified a novel JAK family kinase inhibitor, dehydrocrenatidine, that inhibits JAK-STAT3-dependent DU145 and MDA-MB-468 cell survival and induces cell apoptosis. Dehydrocrenatidine represses constitutively activated JAK2 and STAT3, as well as interleukin-6-, interferon-α-, and interferon-γ-stimulated JAK activity, and STAT phosphorylation, and suppresses STAT3 and STAT1 downstream gene expression. Dehydrocrenatidine inhibits JAKs-JH1 domain overexpression-induced STAT3 and STAT1 phosphorylation. In addition, dehydrocrenatidine inhibits JAK2-JH1 kinase activity in vitro. Importantly, dehydrocrenatidine does not show significant effect on Src overexpression and epidermal growth factor-induced STAT3 activation. Our results indicate that dehydrocrenatidine is a JAK-specific inhibitor.

Although previous studies confirmed that steaming and the fermentation process could significantly improve the cognitive-enhancement and neuroprotective effects of Codonopsis lanceolata, the anti-tumor efficacy of steamed C. lanceolata (SCL) and what mechanisms are involved remain largely unknown. The present study was designed to evaluate the anti-tumor effect in vivo of SCL in H22 tumor-bearing mice. The results clearly indicated that SCL could not only inhibit the tumor growth, but also prolong the survival time of H22 tumor-bearing mice. Besides, the serum levels of cytokines, such as interferon gamma (IFN-γ), tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6) and interleukin-2 (IL-2), were enhanced by SCL administration. The observations of Hoechst 33258 staining demonstrated that SCL was able to induce tumor cell apoptosis. Finally, immunohistochemical analysis revealed that SCL treatment significantly increased Bax expression and decreased Bcl-2 and vascular endothelial growth factor (VEGF) expression of H22 tumor tissues in a dose-dependent manner. Moreover, LC/MS analysis of SCL indicated that it mainly contained lobetyolin and six saponins. Taken all together, the findings in the present study clearly demonstrated that SCL inhibited the H22 tumor growth in vivo at least partly via improving the immune functions, inducing apoptosis and inhibiting angiogenesis.

Brucellosis is a zoonotic infectious disease caused by Brucella infection. MarR-family transcription factors are closely related to diverse physiological functions necessary for many pathogens adaptation to environmental changes. However, whether the MarR-family transcription factors are involved in virulence, mediated inflammatory responses and regulated virulence gene expression in the intracellular pathogen Brucella are still unknown. Therefore, we created a 2308ΔMarR6 mutant of B. abortus 2308 (S2308). Virulence and inflammatory cytokines assays were performed using a murine macrophage cell line (RAW 264.7). We also performed chromatin immunoprecipitation of MarR6 followed by next-generation sequencing (ChIP-seq). The results showed that 2308ΔMarR6 was significantly reduced survival capability in RAW 264.7. After the macrophages were infected with 2308ΔMarR6, the levels of tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), interleukin-6 (IL-6), interleukin-12 (IL-12), interferon-gamma (IFN-γ) and macrophage chemoattractant protein-1 (MCP-1) were decreased and were significantly lower than that for the S2308-infected group, indicating that the 2308ΔMarR6 mutant could reduce the secretion of inflammatory cytokines. Furthermore, we detected 122 intergenic ChIP-seq peaks of MarR6 binding distributed across the Brucella genome. Taken together, the research has recorded valuable data about MarR6. Our findings are of great significance in elucidating the function of MarR6.

CD47 and its receptor signal regulatory protein α (SIRPα) act as a dominant antiphagocytic, "don't eat me" signal. Recent studies reveal CD24 as a novel target for cancer immunotherapy by macrophages in ovarian cancer and breast cancer. However, whether simultaneous blockade of CD47 and CD24 by a bispecific antibody may result in a potential synergy is still unclear. In the present study, we for the first time designed and developed a bispecific antibody fusion protein, PPAB001 for cotargeting CD47 and CD24. Data demonstrate that simultaneous blockade of CD47/SIRPα and CD24/Siglec-10 signaling by PPAB001 potently promoted macrophage phagocytosis of tumor cells. Compared to single CD47 or CD24 targeting agents, PPAB001 was more effective in inhibiting tumor growth in both mouse 4T-1 syngeneic and human SK-OV-3 xenogeneic tumor models. Mechanistically, we found that PPAB001 therapy markedly increased the proportion of tumor-infiltrating macrophages and upregulated interleukin-6 and tumor necrosis factor-α levels that were representative macrophage inflammatory cytokines. Notably, an increased ratio of M1/M2 in tumor-infiltrating macrophages in the mice treated with PPAB001 suggested that the dual blockade may promote the transition of macrophages from M2 to M1. Taken together, our data supported the development of PPAB001 as a novel immunotherapeutic in the treatment of CD47 and CD24 double-positive cancers.

In this study we report on the clinical and autoimmune characteristics of severe and critical novel coronavirus pneumonia caused by severe acute respiratory syndrome-associated coronavirus 2 (SARS-CoV-2). The clinical, autoimmune, and laboratory characteristics of 21 patients who had laboratory-confirmed severe and critical cases of coronavirus disease 2019 (COVID-19) from the intensive care unit of the Huangshi Central Hospital, Hubei Province, China, were investigated. A total of 21 patients (13 men and 8 women), including 8 (38.1%) severe cases and 13 (61.9%) critical cases, were enrolled. Cough (90.5%) and fever (81.0%) were the dominant symptoms, and most patients (76.2%) had at least one coexisting disorder on admission. The most common characteristics on chest computed tomography were ground-glass opacity (100%) and bilateral patchy shadowing (76.2%). The most common findings on laboratory measurement were lymphocytopenia (85.7%) and elevated levels of C-reactive protein (94.7%) and interleukin-6 (89.5%). The prevalence of anti-52 kDa SSA/Ro antibody, anti-60 kDa SSA/Ro antibody, and antinuclear antibody was 20%, 25%, and 50%, respectively. We also retrospectively analyzed the clinical and laboratory data from 21 severe and critical cases of COVID-19. Autoimmune phenomena exist in COVID-19 subjects, and the present results provide the rationale for a strategy of preventing immune dysfunction and optimal immunosuppressive therapy.

Oxidative stress can lead to intestinal cell injury as well as the induction of inflammation. It is not clear whether inflammation is an important factor leading to cell injury caused by oxidative stress. The purpose of this study was to investigate the role of inflammation in intestinal injury caused by hydrogen peroxide (H2O2). Our results revealed that H2O2 stimulation significantly decreased the viability of intestinal porcine epithelial cells (IPEC-1), increased lactate dehydrogenase (LDH) activity, and disrupted the distribution of the tight junction protein claudin-1. H2O2 significantly increased the mRNA expression of interleukin-6 (IL-6), IL-8, and tumor necrosis factor-α (TNF-α). H2O2 stimulation also led to increased phosphorylation of p38 and jun N-terminal kinase (JNK), and p65 NF-κB protein translocation into the nucleus of IPEC-1 cells. Cells treated with the NF-κB inhibitor (BAY11-7082), the p38 inhibitor (SB202190), or the JNK inhibitor (PD98059) significantly decreased mRNA and protein expression of IL-6, IL-8, and TNF-α. However, treatment with mitogen-activated protein kinase (MAPK) or NF-κB inhibitors did not prevent the damage effect on cell viability, LDH activity, or the distribution of claudin-1 in cells challenged with H2O2. In summary, our data demonstrate that activation of the NF-κB and MAPK signaling pathways can contribute to the inflammatory response, but not cell injury, in IPEC-1 cells challenged with H2O2.

Eighty-eight ischemic stroke patients with massive cerebral infarction (MCI) who met our selection criteria were included in this study. MCI was assessed using the Glasgow Coma Scale (GCS) at hospital admission and at 2 weeks. The sera of all patients and controls were sampled at 48 h after the patients' attacks, and the sera of patients with MCI who had no severe cardiopulmonary complications, including those with hemorrhagic transformation (HT), were sampled again at 2 weeks. The relative expression of let-7 miRNA in the serum was determined by real-time qRT-PCR, and the blood levels of lipids, glucose, high-sensitivity C-reactive protein (hs-CRP), homocysteine and blood pressure were measured at admission. Interleukin-6 (IL-6) levels were detected by ELISA, and a luciferase assay was performed to confirm that IL-6 was a gene target of let-7. The relative expression of let-7f was significantly down-regulated in MCI without HT patients compared with controls (P<0.001), and it was positively correlated with GCS (P<0.01) and negatively correlated with hs-CRP (P<0.01). The relative expression of let-7f was significantly up-regulated in MCI patients with HT (P<0.01). IL-6 is a direct target gene for let-7f, and IL-6 expression was increased in MCI without HT patients compared to controls (P<0.01). The expression of let-7f in serum is associated with MCI without HT, which specifically inhibits IL-6. This suggests that let-7f may control inflammation in patients with MCI without HT.

The purpose of the present study was to investigate the differentially expressed proteins between endotoxin tolerance and sepsis. Cell models of an endotoxin tolerance group (ET group) and sepsis group [lipopolysaccharide (LPS) group] were established using LPS and evaluated using ELISA and flow cytometry methods. Differentially expressed proteins between the ET and the LPS groups were identified using isobaric tags for relative and absolute quantitation (iTRAQ) analysis and evaluated by bioinformatics analysis. The expression of core proteins was detected by western blotting. It was identified that the expression of tumor necrosis factor‑α and interleukin‑6 was significantly decreased in the ET group compared with the LPS group. Following high‑dose LPS stimulation for 24 h, the positive rate of cluster of differentiation‑16/32 in the ET group (79.07%) was lower when compared with that of the LPS group (94.27%; P<0.05). A total of 235 proteins were identified by iTRAQ, and 36 upregulated proteins with >1.2‑fold differences and 27 downregulated proteins with <0.833‑fold differences were detected between the ET and LPS groups. Furthermore, the expression of high mobility group (HMG)‑A1 and HMGA2 in the ET group was higher compared with the LPS group following high‑dose LPS stimulation for 4 h, while HMGB1 and HMGB2 exhibited the opposite expression trend under the same conditions. In conclusion, proteomics analysis using iTRAQ technology contributes to a deeper understanding of ET mechanisms. HMGA1, HMGA2, HMGB1 and HMGB2 may serve a crucial role in the development of ET.

Few studies have addressed the mechanism by which circ_0010729 regulates hypoxia-induced cell injury in cardiovascular diseases. However, its role and its regulatory mechanism in myocardial infarction remain to be explored. Cell viability, cycle, apoptosis, and migration were analyzed using cell counting kit-8 assay, flow cytometry, caspase-3 activity assay kit and transwell assay, respectively. Tumor necrosis factor-α (TNF-α), and interleukin-6 (IL-6) concentrations were examined by enzyme-linked immunosorbent assay. Glucose metabolism was calculated by detecting ATP production, glucose uptake and lactate production. Levels of circ_0010729, miR-370-3p and TNF Receptor Associated Factor 6 (TRAF6) were detected using quantitative real-time polymerase chain reaction or western blot. The direct interaction between circ_0010729 and TRAF6 or miR-370-3p was verified using dual-luciferase reporter assay and RNA immunoprecipitation assay. Under hypoxia condition, cardiomyocytes suffered from cell viability suppression, cell cycle arrest, cell apoptosis promotion, migration reduction, increase of inflammatory factor IL-6 and TNF-α, as well as glycolysis inhibition. Circ_0010729 expression was up-regulated in the cardiomyocytes at different hypoxia-exposed time points. Circ_0010729 knockdown protected cardiomyocytes against hypoxic dysfunction, while circ_0010729 overexpression showed inverse effects. MiR-370-3p was confirmed to directly bind to circ_0010729 or TRAF6. MiR-370-3p inhibition attenuated the protective effects of circ_0010729 knockdown on hypoxia-modulated cardiomyocyte dysfunction. MiR-370-3p restoration protected cardiomyocytes against hypoxic injury via targeting TRAF6. Besides, circ_0010729 indirectly regulated TRAF6 expression via miR-370-3p. This study demonstrated that circ_0010729 knockdown attenuated hypoxia-induced cardiomyocyte dysfunction via miR-370-3p/TRAF6 axis, indicating a potential therapeutic target for myocardial infarction.

The aim of the present study was to investigate the association between tubulin folding cofactor B (TBCB) expression and ischemia-reperfusion injury (IRI) in mice. A total of 48 C57BL/6 mice were randomly divided into a control group (Sham, n=6) and an ischemia-reperfusion group (n=42). The ischemia-reperfusion group was further divided into 6 subgroups as per different times after reperfusion (2, 4, 6, 8, 12 and 24 h), with 7 mice per subgroup. A hepatic IRI model was established in mice by clamping the hepatic hilum. Morphology, serum levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), interleukin 6 (IL-6) and tumor necrosis factor-α (TNF-α), and the expression level of TBCB were detected. Compared with the control group, the livers from the ischemia-reperfusion group were significantly changed, particularly at 12 h following ischemia-reperfusion, with obvious hepatic cell degeneration and necrosis. The ALT, AST, IL-6 and TNF-α levels in the sera of the mice in the hepatic ischemia-reperfusion group were increased at all time points following ischemia-reperfusion, and were the highest at 12 h, demonstrating statistically significant differences when compared with the control group (P<0.05). Furthermore, the expression levels of TBCB, TNF-α and IL-6 were significantly increased at all time-points following ischemia-reperfusion, and were the most significant at 12 h. At 24 h following ischemia-reperfusion, the expression levels had decreased. The present study indicated that TBCB expression is associated with TNF-α and IL-6 expression levels in mice with hepatic ischemia-reperfusion, and may be key in the development of liver injury during ischemia-reperfusion in mice.

The aim of this study was to study the preventive effects of polyphenols extracted from Liubao Insect tea on gastric injury. The content of Liubao Insect tea polyphenols (LITP) was 72.36% by ion precipitation extraction method. HCl/ethanol-induced gastric injury in mice led to increased gastric juice volume and decreased pH. LITP increased the gastric juice pH value and reduced the gastric juice volume at slightly lower quantities than ranitidine. Visual observation of gastric tissue showed that LITP could effectively reduce the area of gastric injury, and higher concentrations of LITP had a greater effect. Pathological observation also confirmed that LITP can reduce the cell damage and inflammatory effects, and play a role in preventing gastric injury. Serum cytokine assays showed that LITP could reduce the levels of IL-6 (interleukin 6), TNF-α (tumor necrosis factor alpha) and IFN-γ (interferon gamma) induced by gastric injury, and the effects of higher concentration of LITP were similar to those of ranitidine. The results showed that LITP could increase SOD (superoxide dismutase) and GSH (glutathione) levels; decrease MDA (malondialdehyde) and MPO (myeloperoxidase) levels; up-regulate the expression of Cu/Zn-SOD (cuprozinc-superoxide dismutase), Mn-SOD (manganese superoxide dismutase), CAT (catalase), nNOS (neuronal nitric oxide synthase), eNOS (endothelial nitric oxide synthase); and down-regulate the expression of iNOS (inducible nitric oxide synthase), COX-2 (cyclooxygenase-2), TNF-α, and IL-1β (interleukin-1 beta) in mice with gastric injury, thus inhibiting gastric injury. We demonstrate that LITP is an active substance which could prevent gastric injury in experimental animals. With the increase of LITP concentration, its effects on preventing gastric injury were stronger and similar to those of ranitidine.

Liubao tea is a type of traditional Chinese tea, belonging to the dark teas. This study is a basic research of the contained polyphenols (active substances) and detected preventive effects of polyphenols of raw Liubao tea (PRLT) on mouse gastric injuries induced by HCl/ethanol. High-pressure liquid chromatography was used to analyze the components of PRLT. Furthermore, a mouse gastric injury model was established to observe the preventive effects. PRLT was shown to contain gallic acid, EGC (epigallocatechin), catechin, caffeine, EC (epicatechin), EGCG (epigallocatechin gallate), GCG (gallocatechin gallate), and ECG (epicatechin gallate). The results of the in vivo study indicate that PRLT can inhibit the observed increase of gastric juice volume and decrease of gastric juice pH caused by gastric injury. PRLT can decrease the serum levels of IL-6 (interleukin-6), IL-12 (interleukin-12), TNF-α (tumor necrosis factor-α), and IFN-γ (interferon-γ) in mice with gastric injuries. Moreover, it can also increase the serum levels of SS (somatostatin) and VIP (vasoactive intestinal peptide) and reduce the serum levels of both SP (substance P) and ET-1 (endothelin-1). PRLT was also shown to increase SOD (superoxide dismutase) and GSH (glutathione) levels and decrease MDA (malondialdehyde) level. The detection of mRNA and protein in gastric tissues indicates that PRLT could also up-regulate the expression of Cu/Zn-SOD (copper/zinc superoxide dismutase), Mn-SOD (manganese superoxide dismutase), CAT (catalase), nNOS (neuronal nitric oxide synthase), and eNOS (endothelial nitric oxide synthase) and down-regulate the expression of both iNOS (inducible nitric oxide synthase) and COX-2 (cyclooxygenase-2). Thus, PRLT possess a good preventive effect on gastric injury, which is directly related to the contained active substance. PRLT show good anti-oxidative and preventive effect in gastric injury and offer promising application value.