[Effect and mechanism of acupoint injection on influenza A virus induced pneumonia in mice].

OBJECTIVE: To investigate the effect and mechanism of acupoint injection with 0.1% vitamin C+vitamin B complex solution (VC+VBCo) at "Tiantu" (CV 22), "Quchi" (LI 11) and "Zusanli" (ST 36) in mouse model of pneumonia induced by influenza A virus (A/PR/8/34 [H1N1], PR8). METHODS: Sixty male ICR mice were randomized into 6 groups, i.e. control group, model group, acupoint injection group, intraperitoneal injection group, non-target point group and ribavirin group, 10 mice in each one. Except the control group, the pneumonia models were induced by slow nasal dripping PR8 virus in the other groups. On the 2nd day of experiment, VC+VBCo solution, 40 µL was injected at "Tiantu" (CV 22), "Quchi" (LI 11, left) and "Zusanli" (ST 36, left) in the acupoint injection group; VC+VBCo solution, 120 µL was injected intraperitoneally in the intraperitoneal injection group; VC+VBCo solution, 40 µL was injected at non-target acupoints (0.5 cm away from "Tiantu" [CV 22] to the left side, "Quchi" [LI 11, left] and "Zusanli" [ST 36, left]) in the non-target point group; and ribavirin solution, 120 µL was injected intraperitoneally in the ribavirin group. The intervention was delivered once daily, for consecutive 7 days. Three parallel experiments were undertaken. The mean death rate and survival time were assessed in each group, the body mass and lung index were compared among groups. Using HE staining, the morphology of lung tissue was observed; and with real-time fluorescence quantitative PCR, viral load in lung tissue was detected. The concentrations of inflammatory factors (tumor necrosis factor α [TNF-α], interleukin [IL]-1ß, IL-10) were detected in lung tissue of each group using ELISA; and those of oxidative stress markers (superoxide dismutase [SOD], glutathione peroxidase [GSH-Px], malondialdehyde [MDA]) were detected with chemiluminescence method. RESULTS: Compared with the control group, the body mass was decreased and lung index was increased in the model group (P<0.01). In comparison with the model group, body mass was increased in the acupoint injection group (P<0.05), lung index was reduced in the acupoint injection group the and ribavirin group (P<0.05); the mean death rate was decreased and the mean survival time prolonged in the mice of the acupoint injection group (P<0.01, P<0.05); and the mean death rate was reduced in the mice of the ribavirin group (P<0.05). In the model group, the alveolar structure was not integral, the alveolar septum was thickened, inflammatory cells were infiltrated and red blood cells exudated seriously (P<0.01). Compared with the model group, in the acupoint injection group and the ribavirin group, the alveolar structure was integral, the thickened alveolar septum was alleviated; and the infiltration of inflammatory cells and the exudation of red blood cells were reduced remarkably. The viral load was reduced in the mice of the ribavirin group when compared with the model group (P<0.01). Compared with the control group, the concentrations of TNF-α, IL-1ß and MDA in lung tissue were increased and those of IL-10, SOD and GSH-Px were reduced in the model group (P<0.01). In the acupoint injection group and the ribavirin group, the concentrations of TNF-α, IL-1ß and MDA were reduced in lung tissue and those of IL-10, SOD and GSH-Px were increased (P<0.05, P<0.01) when compared with the model group. CONCLUSION: Acupoint injection with VC+VBCo solution may alleviate inflammatory responses and oxidative stress in lung tissue of the PR8-induced pneumonia mice, improve survival rate and prolong the survival time in the case of no effect of the viral load.

Cangma Huadu granules, a new drug with great potential to treat coronavirus and influenza infections, exert its efficacy through anti-inflammatory and immune regulation.

ETHNOPHARMACOLOGICAL RELEVANCE: Coronavirus and influenza virus infection seriously threaten human health. Cangma Huadu Granules (CMHD) is an in-hospital preparation composed of eight traditional Chinese medicines (TCM), which has been clinically used against COVID-19 in China and may be a promising candidate for the treatment of influenza. However, the role of its treatment urgently needs to be studied. AIM OF THE STUDY: To evaluate the therapeutic effects of CMHD on pneumonia induced by coronavirus (HCoV-229E) and influenza A virus (H1N1/FM1) in mice and explore its mechanism of anti-infection. MATERIALS AND METHODS: Mice were infected with HCoV-229E or H1N1/FM1 virus through the nasal cavity. CMHD (12.1, 6.05 and 3.03 g/kg/d) or the positive control drugs were administered intragastrically. The lung index and histopathological changes were used to evaluate the therapeutic effect of CMHD. The expression of TNF-α, IL-1ß, IL-6 and IL-4 in Serum and the proportion of CD4+ and CD8+ T lymphocytes in peripheral blood were detected to evaluate the anti-inflammatory and immune regulation effects of CMHD, respectively. Furthermore, the levels of p-NF-κBp65/ NF-κB p65, which was the key targets of the NF-κB pathway was analyzed. RESULTS: In HCoV-229E-induced pneumonia, the lung index was markedly reduced, and lung pathology was improved in mice that treated with CMHD (12.1, 6.05 g/kg/d). Meanwhile, the expression of TNF-α, IL-6 were obviously inhibited, but the expression of IL-4 was significantly increased in CMHD groups. Compared with the model group, CMHD could also markedly upregulate the level of CD4+ and CD8+. Furthermore, CMHD has a markedly effect on inhibit the expression of p-NF-κB p65/NF-κB p65 in the lung. In H1N1-induced pneumonia, the lung index of mice in the CMHD (12.1 g/kg/d) treatment group was lower than that in the model group, and less inflammatory infiltration could be seen in the lung pathological. Moreover, CMHD could also obviously decrease the expression of TNF-α, IL-1ß, IL-6, but significantly increase the expression of IL-4. Except for that, CMHD could also markedly downregulate the level of CD4+ and upregulate the level of CD8+ compared with the model group. In addition, CMHD has a markedly effect on inhibit the expression of p-NF-κB p65/NF-κB p65 in the lung. CONCLUSION: CMHD can significantly combats viral infections caused by HCoV-229E and H1N1, and the mechanism may be related to its multiple functions of anti-inflammatory, immunity regulating and inhibiting NF-κB signal transduction pathway.

A rare occurrence of a hereditary Birt-Hogg-Dubé syndrome: A case report.

BACKGROUND: Birt-Hogg-Dubé (BHD) syndrome is a rare autosomal dominant disease caused by germline mutations in the folliculin (FLCN) protein gene, which usually manifests as cutaneous fibrofolliculoma, pulmonary cysts, renal cell carcinoma, and spontaneous pneumothorax. CASE SUMMARY: A 26-year-old woman with no history of smoking was admitted to the Respiratory Department of our hospital due to intermittent wheezing that lasted for 8 mo. She had experienced recurrent spontaneous pneumothorax more than four times during the past 8 mo. After admission, the patient again suffered from left pneumothorax without a clear reason. Lung computed tomography (CT) showed multiple low-density cystic changes in both lungs. Physical examination on admission revealed multiple white dome-shaped papules in the neck, the nape, and behind the ear. In addition, the patient had a family history of spontaneous pneumothorax. Her mother had suffered from pneumothorax four times (at age 36, 37, 42, and 50 years). Her second maternal aunt had suffered from a right pneumothorax at the age of 40. The multidisciplinary diagnosis of BHD, which included the Respiratory Department, Radiology Department, Pathology Department, and Dermatological Department, was BHD and was later confirmed by family genetic testing. The same variation (FLCN gene) was found in the patient's mother and aunt. CONCLUSION: This case highlights the importance of multidisciplinary diagnosis and a treatment platform for the diagnosis of BHD.

Amplification of DDR2 mediates sorafenib resistance through NF-κB/c-Rel signaling in hepatocellular carcinoma.

Sorafenib was the first systemic therapy approved by the Food and Drug Administration to treat advanced hepatocellular carcinoma (HCC). However, sorafenib therapy is frequently accompanied by drug resistance. We aimed to explore the mechanisms of sorafenib resistance and provide feasible solutions to increase the response to sorafenib in patients with advanced HCC. The expression profile of discoidin domain receptor 2 (DDR2) in HCC tissues and cells was detected using quantitative real-time PCR (qPCR) and western blotting assays. The effects of DDR2 on sorafenib resistance were examined using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide, colony formation, TdT-mediated dUTP nick end labeling, and flow cytometry assays. The effect of DDR2 on the nuclear factor kappa B (NF-κB) signaling pathway was evaluated by luciferase reporter, immunofluorescence, qPCR and flow cytometry assays. We demonstrated that DDR2 expression was dramatically upregulated in sorafenib-resistant HCC tissues relative to sensitive tissues. Downregulation of DDR2 sensitized HCC cell lines to sorafenib cytotoxicity. Further analysis showed that DDR2 could increase the nuclear location of REL proto-oncogene, a NF-κB subunit, to mediate NF-κB signaling. Blocking NF-κB signaling using the NF-κB signaling inhibitor, bardoxolone methyl, increased the response of HCC cells to sorafenib. Further analysis showed that DNA amplification of DDR2 is an important mechanism leading to DDR2 overexpression in HCC. Our results demonstrated that DDR2 is a potential therapeutic target in patients with HCC, and targeting DDR2 represents a promising approach to increase sorafenib sensitivity in patients with HCC.

The effectiveness of electro-acupuncture combined with dyclonine hydrochloride in relieving the side effects of gastroscopy: a controlled trial.

BACKGROUND: The present study aimed to explore the effectiveness of electro-acupuncture (EA) in combination with a local anesthetic used in Western medicine in preventing the side effects of gastroscopy. METHODS: A sample group of 150 patients were divided into three groups based on treatment methods: an EA group, a dyclonine hydrochloride mucilage group, and a combined treatment group. In the EA group, EA stimulation was given at the Hegu, Neiguan, and Zusanli acupoints; in the dyclonine hydrochloride mucilage group, patients took 10 mL of dyclonine hydrochloride mucilage orally; in the combined treatment group, prevention of side effects was attempted by administration of both acupuncture and oral local anesthetic. The incidences of nausea, emesis, salivation, cough, restlessness, and breath holding during gastroscopy were observed and recorded for the three groups. Mean arterial pressure, heart rate, and oxygen saturation were recorded before the examination, and changes in these measures were recorded as the gastroscope passed through the pylorus and after the examination. The visual analogue scale (VAS) values of nausea and emesis, the rate of successful first-pass intubation, and the time of gastroscopy were also recorded. Statistical analysis was performed using R-3.5.3 software. RESULTS: Incidences of side effects (e.g., nausea, emesis, salivation, restlessness, and breath holding) during the examination were lower in the combined treatment group than in the EA group and the dyclonine hydrochloride mucilage group (P<0.05 and P<0.01, respectively). Furthermore, the changes in heart rate and oxygen saturation when the gastroscope passed through the pylorus and after the examination were better in the combined treatment group than in the EA group and dyclonine hydrochloride mucilage group (P<0.01). The VAS values of nausea and emesis, the first-pass success rate, and examination duration were also better for the combined treatment group than for the other two groups (P<0.05 and P<0.01). CONCLUSIONS: EA combined with local anesthesia with dyclonine hydrochloride mucilage can alleviate side effects during gastroscopy, reduce patient pain, and improve the efficiency of the procedure.

Cytokines and their relationship with the severity and prognosis of coronavirus disease 2019 (COVID-19): a retrospective cohort study.

OBJECTIVE: To delineate the characteristics and clinical significance of plasma inflammatory cytokines altered in COVID-19. DESIGN: Retrospective, single-centre cohort study. SETTING: Tongji Hospital in Wuhan, China. PARTICIPANTS: Among a cohort of 308 patients with a diagnosis of COVID-19, 138 patients died while 170 patients recovered and were discharged from the hospital. The data were collected until 27 February 2020. PRIMARY AND SECONDARY OUTCOME MEASURES: Clinical characteristics and laboratory findings were obtained from electronic medical records using data collection forms. RESULTS: The percentage of patients with elevated interleukin 2 receptor (IL-2R), IL-6, IL-8, IL-10 and tumour necrosis factor (TNF) increased with severity of disease (p<0.0001 for all). IL-2R (p<0.0001), IL-6 (p<0.0001), IL-8 (p=0.0001), IL-10 (p<0.0001) and TNF (p<0.0001) were also twofold to 20-fold higher in patients who died compared with those who recovered. Also, IL-6 and IL-10 increased in both the progressive patient groups: moderate (p=0.0026) and severe (p<0.0001). In multivariate analysis, higher levels of IL-2R (OR 1.001, 95% CI 1.000 to 1.002, p=0.031) and IL-6 (OR 1.013, 95% CI 1.003 to 1.024, p=0.015) on admission were associated with increasing odds of in-hospital death, independent of other covariates, including severity of disease and lymphocyte count. CONCLUSION: Increased proinflammatory and anti-inflammatory cytokines, including IL-2R, IL-6, IL-8, TNF and IL-10, showed an obvious association with both COVID-19 severity and in-hospital mortality. Thus, our study indicates that cytokines are valuable in predicting the severity of COVID-19 and helps in distinguishing critically ill patients from the less affected ones.

Aryl hydrocarbon receptor activation mediates kidney disease and renal cell carcinoma.

The aryl hydrocarbon receptor (AhR) is a well-known ligand-activated cytoplasmic transcription factor that contributes to cellular responses against environmental toxins and carcinogens. AhR is activated by a range of structurally diverse compounds from the environment, microbiome, natural products, and host metabolism, suggesting that AhR possesses a rather promiscuous ligand binding site. Increasing studies have indicated that AhR can be activated by a variety of endogenous ligands and induce the expression of a battery of genes. AhR regulates a variety of physiopathological events, including cell proliferation, differentiation, apoptosis, adhesion and migration. These new roles have expanded our understanding of the AhR signalling pathways and endogenous metabolites interacting with AhR under homeostatic and pathological conditions. Recent studies have demonstrated that AhR is linked to cardiovascular disease (CVD), chronic kidney disease (CKD) and renal cell carcinoma (RCC). In this review, we summarize gut microbiota-derived ligands inducing AhR activity in patients with CKD, CVD, diabetic nephropathy and RCC that may provide a new diagnostic and prognostic approach for complex renal damage. We further highlight polyphenols from natural products as AhR agonists or antagonists that regulate AhR activity. A better understanding of structurally diverse polyphenols and AhR biological activities would allow us to illuminate their molecular mechanism and discover potential therapeutic strategies targeting AhR activation.

Gut microbiota in obstructive sleep apnea-hypopnea syndrome: disease-related dysbiosis and metabolic comorbidities.

Gut microbiota alterations manifest as intermittent hypoxia and fragmented sleep, thereby mimicking obstructive sleep apnea-hypopnea syndrome (OSAHS). Here, we sought to perform the first direct survey of gut microbial dysbiosis over a range of apnea-hypopnea indices (AHI) among patients with OSAHS. We obtained fecal samples from 93 patients with OSAHS [5 < AHI ≤ 15 (n=40), 15 < AHI ≤ 30 (n=23), and AHI ≥ 30 (n=30)] and 20 controls (AHI ≤ 5) and determined the microbiome composition via 16S rRNA pyrosequencing and bioinformatics analysis of variable regions 3-4. We measured fasting levels of homocysteine (HCY), interleukin-6 (IL-6), and tumor necrosis factor α (TNF-α). Results revealed gut microbial dysbiosis in several patients with varying severities of OSAHS, reliably separating them from controls with a receiver operating characteristic-area under the curve (ROC-AUC) of 0.789. Functional analysis in the microbiomes of patients revealed alterations; additionally, decreased in short-chain fatty acid (SCFA)-producing bacteria and increased pathogens, accompanied by elevated levels of IL-6. Lactobacillus levels correlated with HCY levels. Stratification analysis revealed that the Ruminococcus enterotype posed the highest risk for patients with OSAHS. Our results show that the presence of an altered microbiome is associated with HCY among OSAHS patients. These changes in the levels of SCFA affect the levels of pathogens that play a pathophysiological role in OSAHS and related metabolic comorbidities.

Effects of three IL-15 variants on NCI-H446 cell proliferation and expression of cell cycle regulatory molecules.

Interleukin 15 (IL-15) is a cytokine exhibiting antitumor characteristic similar to that of IL-2. However, in human tissues and cells, IL-15 expression and secretion is very limited, suggesting IL-15 functions mainly intracellularly. In the present study, we assessed the effects of transfecting NCI-H446 small cell lung cancer cells with genes encoding three IL-15 variants: prototypical IL-15, mature IL-15 peptide, and modified IL-15 in which the IL-2 signal peptide is substituted for the native signal peptide. NCI-H446 cells transfected with empty plasmid served as the control group. We found that IL-15 transfection effectively inhibited NCI-H446 cell proliferation and arrested cell cycle progression, with the modified IL-15 carrying the IL-2 signal peptide exerting the greatest effect. Consistent with those findings, expression each of the three IL-15 variants reduced growth of NCI-H446 xenograph tumors, and the modified IL-15 again showed the greatest effect. In addition, IL-15 expression led to down-regulation of the positive cell cycle regulators cyclin E and CDK2 and up-regulation of the negative cycle regulators p21 and Rb. These findings suggest IL-15 acts as a tumor suppressor that inhibits tumor cell proliferation by inducing cell cycle arrest.

Decreased DACH1 expression in glomerulopathy is associated with disease progression and severity.

Cell fate determination factor dachshund1 (DACH1) is a chromosome-associated protein that regulates cellular differentiation throughout development. Recent genome-wide association studies have show that missense mutation in DACH1 leads to hereditary renal hypodysplasia. Renal DACH1 expression can be used to estimate glomerular filtration rate (eGFR). We firstly characterized the function of DACH1 in normal and diseased renal tissue using immunohistochemistry to assess DACH1 in human renal biopsy specimens from 40 immunoglobulin A nephropathy (IgAN) patients, 20 idiopathic membranous nephropathy (IMN) patients, and 15 minimal change disease (MCD) patients. We found that DACH1 expression was decreased in the nephropathy group relative to healthy controls. DACH1 staining in the glomerulus correlated positively with eGFR (r = 0.41, p < 0.001) but negatively with serum creatinine (r = -0.37, p < 0.01). In vitro, DACH1 overexpression in human podocytes or HK2 cells decreased expression of cyclin D1, but increased expression of p21 and p53, which suggested that DACH1 overexpression in human podocytes or HK2 cells increased the G1/S phase or G2/M cell arrest. Together, These findings indicate that DACH1 expression is decreased in glomerulopathy imply a potential role for DACH1 in the this development of human chornic glomerulopathy. These data suggest that DACH1 is a potential a marker of disease progression and severity for glomerular diseases.

Changes in levels of T cell subpopulations to monitor the response to antiretroviral therapy among HIV-1-infected patients during two years of HIV-1 replication suppression.

OBJECTIVES: The aim of this study was to compare the effect of 2 y of antiretroviral therapy (ART) on the percentage of activated CD38⁺CD8⁺ T cells and human leukocyte antigen (HLA)-DR⁺CD8⁺ T cells, and the expression of the co-stimulatory molecule CD28 on CD4⁺ and CD8⁺ T cells in the peripheral blood of HIV-infected adults, and to assess the use of immune activation markers to predict the virological response to ART in a cohort of HIV-1-infected patients in the north-western part of China. METHODS: We analyzed changes in the CD4⁺ T cell count, viral load, and the percentages of CD38⁺CD8⁺ T cells, HLA-DR⁺CD8⁺ T cells, CD28⁺CD4⁺ T cells, and CD28⁺CD8⁺ T cells in 48 patients with HIV diseases during 2 y of suppressive highly active antiretroviral therapy (HAART). Good virological responders (n = 20) were defined as those who had suppressed and maintained a plasma viral load below the detection limit of the assay for at least 12 months. Poor virological responders (n = 28) were defined as those with a detectable viral load at 6 and 12 months after beginning HAART. RESULTS: Among the 20 good responders, baseline median levels of CD38⁺CD8⁺ T cells were elevated, but had decreased significantly at 24 months of therapy (p < 0.0001). Median levels of HLA-DR⁺CD8⁺ T cells also decreased at 24 months of therapy (p < 0.0001). Levels of expression of CD28⁺CD4⁺ T cells rose steadily to 6 months (p = 0.03), and smoothly reached levels observed among HIV-negative blood donors during the 24 months of therapy (p > 0.05). Levels of expression of CD28⁺CD8⁺ T cells increased at 24 months (p = 0.04). Among the 28 poor responders, median levels of CD38⁺CD8⁺ T cells decreased significantly at 24 months (p < 0.0001). Levels of HLA-DR⁺CD8⁺ T cells also decreased at 24 months (p < 0.001). Levels of CD28⁺CD8⁺ T cells and levels of CD28⁺CD4⁺ T cells increased at 24 months remained unchanged. The percentage of CD38⁺CD8⁺ T cells appeared to provide a sensitive estimate of the overall immune recovery in comparison with the percentage of HLA-DR⁺CD8⁺ T cells, although this lacked specificity for the determination of early virological drug failure and did not appear to be a reliable surrogate for RNA viral load. CONCLUSIONS: We show that HAART can be used successfully in Chinese populations with elevated baseline immune activation markers and that the percentage of CD38⁺CD8⁺ T cells may be an additional parameter to the current criteria for estimating the antiretroviral response with HAART.

[Clinical value of 64-slice spiral 3-phase CT enhanced scanning for preoperative TNM staging assessment of gastric carcinoma].

OBJECTIVE: To explore the clinical value of 64-slice spiral 3-phase CT enhanced scanning for preoperative TNM staging assessment of gastric carcinoma. METHODS: A retrospective study was performed to review the 64-slice spiral 3-phase CT enhanced scanning of 120 patients with gastric cancer diagnosed by biopsy prior to operation and postoperative pathological reports. All the findings were reviewed by two senior radiologic diagnosticians separately and compared with pathological findings. RESULTS: The accuracy of 64-slice spiral CT enhanced scan was 79.2%(95/120) for T staging, 66.7%(10/15) for T1, 66.7%(14/21) for T2, 84.0%(42/50) for T3, and 85.3%(29/34) for T4. For gastric wall with single layer and multiple layers, the accuracy of CT enhanced scanning was 59.4%(19/32) and 81.8%(72/88) for T staging, and the difference was statistically significant(P<0.05). The accuracy of 64-slice spiral CT enhanced scan was 73.9%(85/115) for N staging, 75.5%(37/49) for N0, 70.3%(26/37) for N1, 75.9%(22/29) for N2. The accuracy of 64-slice spiral CT enhanced scanning was 89.2% for M staging. CONCLUSION: 64-slice spiral CT 3-phase enhanced scanning can monitor the invasion, lymphatic metastasis, and distant metastasis of gastric cancer dynamically, which may become an important examination item for the preoperative evaluation of gastric cancer.

Toll-like receptor 4 siRNA attenuates LPS-induced secretion of inflammatory cytokines and chemokines by macrophages.

Toll-like receptor 4 (TLR4) is critical for activation of macrophages by Lipopolysaccharide (LPS). In this study, we investigated the silencing effects of TLR4-specific 21-nt small interfering RNAs (siRNA) on TLR4 expression in RAW264.7 cells. It was found that treatment with TLR4 siRNA down-regulated the TLR4 mRNA and protein expression in macrophage RAW264.7 cells, and reduced the sensitivity of the cells to LPS stimulation. Our findings also demonstrate that treatment with TLR4 siRNA significantly decreased the tumor necrosis factor-alpha (TNF-alpha) and macrophage inflammatory protein 2 (MIP-2) expression induced by LPS. TLR4 siRNA treatment also impaired the signalling of mitogen-activated protein kinases (MAPK) induced by LPS in RAW264.7 cells. These data suggest that inhibition of TLR4 expression by TLR4 siRNA may be therapeutically beneficial in controlling the overall responses of immune cells to LPS.

[Protective effects of Xuebijing injection on kidney in rats with sepsis].

OBJECTIVE: To investigate the protective effects of the integrated traditional Chinese and Western medicine Xuebijing injection on the kidney in rats with sepsis. METHODS: Sepsis model was reproduced in rats with cecal ligation and puncture (CLP). Eighty healthy Wistar rats were randomly divided into four groups: control group, sham-operation group, CLP model group, and Xuebijing group. The two latter groups were divided into four groups of 2, 8, 24, 48-hour subgroups with 8 rats in each subgroup. Serum levels of creatinine (Cr), blood urea nitrogen (BUN), Na(+), K(+) were measured. beta (2)-microglobulin (beta (2)-MG) was determined by radioimmunoassay, urine level of Cr, Na(+), interleukin-6 (IL-6) levels in renal tissue, and fractional excretion of sodium (FENa) were determined by enzyme linked immunoadsorbent assay (ELISA). Light microscopy was used to assess the pathological changes in kidney. RESULTS: Compared with CLP model group,the level of beta (2)-MG was significantly decreased at 2 hours in Xuebijing group (P<0.01). Similarly, serum BUN content, renal IL-6 level were lowered at 8 hours, and serum contents of BUN as well as Cr were also decreased in Xuebijing group than those in model group at 48 hours after CLP (P<0.05 or P<0.01). CONCLUSION: Xuebijing injection possesses the protective effects on the kidney in rats with sepsis, which may be related with the synthesis and release of IL-6.