低剂量紫杉醇对膀胱出口部分梗阻后膀胱形态变化的影响

 目的:探讨低剂量紫杉醇对膀胱出口部分梗阻（BOO）大鼠膀胱形态变化的影响。方法:健康雌性Sprague-Dawley大鼠30只,随机分为空白对照组、BOO组和紫杉醇组。BOO组和紫杉醇组行尿道近端梗阻方式制备膀胱出口部分梗阻模型,空白对照组采用假手术方式处理。紫杉醇组于术后给予紫杉醇(溶于生理盐水)腹腔注射（0.3 mg/kg）,每周2次。空白对照组与BOO组以等体积生理盐水同时间腹腔注射。4周后测量体重及膀胱重量,HE染色观察膀胱肌层增生情况;Masson三色染色观察并评价胶原纤维沉积;透射电镜观察逼尿肌超微结构改变。结果:与空白对照组相比,BOO组膀胱重量明显增加（0.376 g±0.052 g vs0.112 g±0.014 g, P<0.05）,膀胱逼尿肌明显增厚,胶原纤维面积占胶原与肌组织面积之和的比值下降（29.66％±2.69％ vs38.94％±3.67％, P<0.05）,电镜下细胞中间连接明显减少,出现丰富的突触连接与桥粒连接,肌细胞间隙内有大量的胶原纤维。与BOO组相比,紫杉醇组膀胱重量显著降低（0.215 g±0.025 g vs0.376 g±0.052 g, P<0.05）,膀胱逼尿肌厚度减小,胶原纤维染色面积占胶原与肌组织面积之和的比值下降（19.94%±1.90% vs29.66%±2.69%, P<0.05）,细胞间连接以中间连接为主,细胞间隙内胶原纤维减少。结论: 低剂量紫杉醇对BOO后膀胱形态结构的变化有一定的修复或逆转作用。     

Time dependent bladder apoptosis induced by acute bladder outlet obstruction and subsequent emptying is associated with decreased MnSOD expression and Bcl-2/Bax ratio

Ischemia/reperfusion (I/R) injury-induced oxidative stress plays an important role in the functional impairment of the bladder following acute bladder outlet obstruction (BOO) via induction of apoptosis. The purpose of this study was to investigate the time course of the bladder apoptosis, and apoptosis related molecular changes in the early stage of acute BOO. Twelve-week-old male Sprague Dawley rats were divided into control, acute BOO only (I), and acute BOO plus subsequent emptying (I/R) for 30, 60, 120 min, 3 days and 2 weeks. We examined the extent of bladder apoptosis, expression of Mn-superoxide dismutase (Mn-SOD), Bcl-2, Bax, caspase 3 and poly (ADP-ribose) (PAR) in the bladder. Bladder apoptosis was significantly increased in the I/R group at 30, 60, and 120 min following bladder emptying. BOO plus subsequent emptying for 30, 60, 120 min showed significant decrease in MnSOD and Bcl-2 expression, and significant increase in caspase 3, Bax expression, and amounts of PAR. These results indicate that bladder apoptosis, induced by acute BOO and subsequent emptying, is associated with decreased MnSOD expression, increased PARP activity and imbalance in apoptosis pathways.     

The effect of testosterone alone and testosterone + estradiol therapy on bladder functions and smooth muscle/collagen content in surgically menopause induced rats

ObjectivesThe aim of the study was to investigate the effect of testosterone alone and testosterone + estradiol therapy on bladder functions and smooth muscle/collagen content in surgically menopause induced rat model.MethodsThe study included 34 female Sprague-Dawley rats, and the rats were divided into four groups. After bilateral oophorectomy, during a 60 days period, six rats received IM saline injection for one time, as a control group, and nine rats received testosterone undecanoate 100 mg/kg IM for one time, and nine rats received testosterone undecanoate 100 mg/kg IM for one time + daily 0.50 mg nasal spray of 17β estradiol. Ten rats were taken as sham group. Urodynamic studies were performed in all groups before and after the study. The rats were sacrificed after 60 days, and cystometric findings and smooth muscle/collagen ratio of the bladders were compared between the groups.ResultsIncrease in maximal bladder capacity and compliance were significantly higher in the testosterone treatment group and testosterone + estradiol treatment group than in the control group (p = 0.01 and p = 0.002, respectively for bladder capacity; p = 0.04 and p = 0.005, respectively for bladder compliance). Smooth muscle/collagen ratio of the bladders was significantly higher in the testosterone and testosterone + estradiol treatment groups than in the control group (p = 0.04 and p = 0.008, respectively).ConclusionsThis study shows that bladder functions may deteriorate in postmenopausal period. In addition to estrogen replacement therapy, testosterone has a significant role to increase bladder smooth muscle, leading to improvement in bladder functions in postmenopausal women with urogenital system dysfunction.     

Investigation of early protein changes in the urinary bladder following partial bladder outlet obstruction by proteomic approach

We investigated the pathophysiological mechanism by proteomic approach as a possible tool to detect the marker proteins to develop lower urinary tract symptoms following bladder outlet obstruction (BOO). Rats were randomized into 3 groups; control, sham operation and BOO groups. BOO group was divided into 1, 3, and 5 day-group. Conventional proteomics was performed with high resolution 2-D gel electrophoresis followed by computational image analysis and protein identification using mass spectrometry using rat urinary bladders. A comparison of bladder of BOO group with control bladder showed that three proteins of optineurin, thioredoxin and preprohaptoglobin were over-expressed in the bladder of BOO group. In addition, four proteins, such as peroxiredoxin 2, transgelin, hippocampal cholinergic neurostimulating peptide (HCNP) and beta-galactoside-binding lectin, were under-expressed in the bladder of BOO group. These data supported that downregulation of HCNP might make detrusor muscle be supersensitive to acetylcholine, up-regulation of optineurin means the protection of nerve injury, and down-regulation of transgelin means the decreased contractility of detrusor muscle. Beside these proteins, other proteins are related to oxidative stress or have a nonspecific function in this study. However more information is needed in human bladder tissue for clinical usage.     

Persistent overexpression of SERCA2a affects bladder functions under physiological conditions, but not in bladder outlet obstruction-induced sub-acute pathological conditions

A functional impairment of the bladder and heart in a decompensated state caused by a pressure overload is accompanied by a decrease in the sarcoplasmic reticulum Ca²⁺-ATPase (SERCA2). The beneficial effects of SERCA2 overexpression in preserving cardiac functions have been previously reported. The aim of the present study was to investigate the effects of overexpressed SERCA2 on bladder functions under physiological and pathological conditions using partial bladder outlet obstruction (BOO) in SERCA2a transgenic Wistar rats (TG). Bladder cystometry and western blot analysis were performed using the wild-type Wistar rats (WT), TG, and BOO models (WTBOO and TGBOO). Persistent overexpression of SERCA2 induces reduced bladder compliance without hypertrophy in TG. BOO induces reduced bladder compliance and hypertrophy in WT and TG in the sub-acute phase, but persistent overexpression of SERCA2a in TG does not aggravate the bladder compliance and hypertrophy. In conclusion, SERCA2a overexpression affects bladder functions under physiological conditions, but not in BOO-induced sub-acute pathological conditions.     

Involvement of hypoxia-triggered endoplasmic reticulum stress in outlet obstruction-induced apoptosis in the urinary bladder

In bladder outlet obstruction (BOO), mechanical stress and ischemia/hypoxia are implicated in structural and functional alterations of the urinary bladder. Because mechanical stress and hypoxia may trigger endoplasmic reticulum (ER) stress, we examined involvement of ER stress in the damage of the bladder caused by BOO. An experimental model of BOO was established in rats by complete ligature of the urethra for 24 h, and bladders were subjected to northern blot analysis and assessment of apoptosis. Isolated urinary bladders and bladder-derived smooth muscle cells (BSMCs) were also exposed to mechanical strain and hypoxia and used for analyses. To examine involvement of ER stress in the damage of the bladder, the effects of a chemical chaperone 4-phenylbutyrate (4-PBA) were evaluated in vitro and in vivo. Outlet obstruction for 24 h induced expression of ER stress markers, GRP78 and CCAAT/enhancer-binding protein-homologous protein (CHOP), in the bladder. It was associated with induction of markers for mechanical stress (cyclooxygenases 2) and hypoxia (vascular endothelial growth factor and glyceraldehyde-3-phosphate dehydrogenase). When isolated bladders and BSMCs were subjected to mechanical strain, induction of GRP78 and CHOP was not observed. In contrast, when BSMCs were exposed to hypoxic stress caused by CoCl2 or thenoyltrifluoroacetone (TTFA), substantial upregulation of GRP78 and CHOP was observed, suggesting involvement of hypoxia in the induction of ER stress. In the bladder subjected to BOO, the number of terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling-positive cells increased in the epithelial cells and BSMCs. Similarly, treatment with TTFA or CoCl2 induced apoptosis of BSMCs, and 4-PBA significantly attenuated ER stress and apoptosis triggered by these agents. Furthermore, in vivo administration with 4-PBA significantly reduced apoptosis in the bladder subjected to BOO. These results suggested that outlet obstruction caused ER stress via hypoxic stress in the bladder and that hypoxia-triggered ER stress may be involved in the induction of apoptosis in BOO.     

A gap junction blocker inhibits isolated whole bladder activity in normal rats and rats with partial bladder outlet obstruction

We examined the effect of 18alpha-glycyrrhetinic acid (18alpha-GA), a gap junction blocker, or propiverine hydrochloride on the activity of isolated whole bladders obtained from intact rats and rats with partial bladder outlet obstruction (BOO). Thirty-two female Sprague-Dawley rats were divided into an intact group and a BOO group. The whole bladder was harvested from each rat and isovolumetric cystometry was performed in Krebs solution. Changes of bladder activity were recorded after addition of 18alpha-GA or propiverine hydrochloride to the perfusate. Propiverine hydrochloride inhibited the amplitude and duration of contraction in both intact and BOO groups. Propiverine hydrochloride also reduced the baseline bladder pressure in the BOO group, but not in the intact group. In contrast, 18alpha-GA inhibited the amplitude and duration of bladder contraction, and also reduced the baseline pressure, in both intact and BOO groups. BOO bladders showed inhibition of the amplitude and duration of bladder contraction at lower concentrations of 18alpha-GA than intact bladders. A gap junction blocker suppressed the in vitro activity of BOO bladders more effectively than that of intact bladders. Therefore, inhibition of intercellular communication in the bladder via gap junctions may be useful for treating detrusor overactivity, as well as propiverine hydrochloride.     

Dietary macronutrients modulate hypertrophy and contractility of the detrusor in an experimental model of bladder obstruction

Objectives

To investigate the effects of various diets on structure and function of the bladder in both normal and obstructed bladders of male Wistar rats.

Restoration of bladder contraction by bone marrow transplantation in rats with underactive bladder

We attempted to increase bladder contraction by bone marrow cell transplantation in rats with underactive bladder due to bladder outlet obstruction (BOO). Twelve female rats were anesthetized with halothane to create BOO. After 1 month, the urethral obstruction was removed and they were divided into a transplant group and a sham-operated group (n = 6 each). Bone marrow cells (1 x 10(7) / 0.2 mL) isolated from green fluorescent protein transgenic rats were injected into the bladder wall of the transplant group. Rats from the sham-operated group received injection of culture medium alone. One month after transplantation, isovolumetric cystometry parameters and histological features of bladder were observed as well as intact control rats (n = 6). The amplitude of bladder contractions was larger and the interval between contractions was shorter in the transplant group than the sham-operated group, and there were no differences in these parameters between the transplant group and the control group. Some green fluorescent muscle layers were found in the bladder wall of the transplant group, and these layers were also labeled by anti alpha-smooth muscle actin antibody. These results suggest that transplanted bone marrow cells may improve bladder contractility by differentiating into smooth muscle-like cells.     

Darapladib,a Lipoprotein-Associated Phospholipase A2 Inhibitor,Reduces Rho Kinase Activity in Atherosclerosis

PurposeIncreased lipoprotein-associated phospholipase A2 (Lp-PLA2) activity and Rho kinase activity may be associated with atherosclerosis. The principal aim of this study was to examine whether darapladib (a selective Lp-PLA2 inhibitor) could reduce the elevated Lp-PLA2 and Rho kinase activity in atherosclerosis.ResultsThe serum levels of triglycerides, total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), high-sensitivity C-reactive protein (hs-CRP), and Lp-PLA2, significantly increased in atherosclerosis model groups, as did Rho kinase activity and cardiomyocyte apoptosis (p<0.05 vs. sham group), whereas nitric oxide (NO) production was reduced. Levels of TC, LDL-C, CRP, Lp-PLA2, and Rho kinase activity were respectively reduced in darapladib groups, whereas NO production was enhanced. When compared to the low-dose darapladib group, the reduction of the levels of TC, LDL-C, CRP, and Lp-PLA2 was more prominent in the high-dose darapladib group (p<0.05), and the increase of NO production was more prominent (p<0.05). Cardiomyocyte apoptosis of the high-dose darapladib group was also significantly reduced compared to the low-dose darapladib group (p<0.05). However, there was no significant difference in Rho kinase activity between the low-dose darapladib group and the high-dose darapladib group (p>0.05).ConclusionDarapladib, a Lp-PLA2 inhibitor, leads to cardiovascular protection that might be mediated by its inhibition of both Rho kinase and Lp-PLA2 in atherosclerosis.     

黄芪注射液对脑缺血再灌注大鼠海马神经元凋亡及JNK3表达的影响

目的:观察黄芪注射液对脑缺血再灌注大鼠海马神经元凋亡及c-Jun N末端激酶3(JNK3)表达的影响。方法:四血管阻断法制备脑缺血再灌注大鼠模型。设假手术组、脑缺血再灌注模型组(模型组)、脑缺血再灌注模型+黄芪注射液组(黄芪注射液组)和脑缺血再灌注模型+黄芪注射液溶剂对照组(溶剂对照组)。除假手术组外其余3组根据再灌注时间不同又分为0 h、0.5 h、2 h、6 h、24 h、72 h和120 h 7个亚组。采用TUNEL法检测海马神经元凋亡,Western blotting法检测海马组织JNK3蛋白变化,real-time PCR法检测海马组织JNK3 mRNA 的表达变化。结果:与假手术组比,模型组大鼠各个时点凋亡细胞数均增多(P<0.05);与模型组比,黄芪注射液组各个时点的细胞凋亡数明显减少(P<0.05),而黄芪注射液溶剂对照组各个时点的细胞凋亡数无明显变化(P>0.05)。除120 h外,模型组各时点海马组织JNK3蛋白及mRNA表达均较假手术组增加(P<0.05);与模型组相比,黄芪注射液可减弱除120 h之外的各时点JNK3 蛋白及mRNA的表达(P<0.05),而黄芪注射液溶剂对照组则无明显变化(P>0.05)。结论:黄芪注射液可抑制脑缺血再灌注大鼠海马神经元凋亡,其抗凋亡机制可能与下调JNK3 mRNA及蛋白表达有关。     

Molecular mechanisms of bladder outlet obstruction in transgenic male mice overexpressing aromatase (Cyp19a1)

We investigated the etiology and molecular mechanisms of bladder outlet obstruction (BOO). Transgenic (Tg) male mice overexpressing aromatase (Cyp19a1) under the ubiquitin C promoter in the estrogen-susceptible C57Bl/6J genetic background (AROM+/6J) developed inguinal hernia by 2 months and severe BOO by 9 to 10 months, with 100% penetrance. These mice gradually developed uremia, renal failure, renal retention, and finally died. The BOO bladders were threefold larger than in age-matched wild-type (WT) males and were filled with urine on necropsy. Hypotrophic smooth muscle cells formed the thin detrusor urinae muscle, and collagen III accumulation contributed to the reduced compliance of the bladder. p-AKT and ERα expression were up-regulated and Pten expression was down-regulated in the BOO bladder urothelium. Expression of only ERα in the intradetrusor fibroblasts suggests a specific role of this estrogen receptor form in urothelial proliferation. Inactivation of Pten, which in turn activated the p-AKT pathway, was strictly related to the activation of the ERα pathway in the BOO bladders. Human relevance for these findings was provided by increased expression of p-AKT, PCNA, and ERα and decreased expression of PTEN in severe human BOO samples, compared with subnormal to mild samples. These findings clarify the involvement of estrogen excess and/or imbalance of the androgen/estrogen ratio in the molecular pathogenetic mechanisms of BOO and provide a novel lead into potential treatment strategies for BOO.     

远期缺血预适应激活热休克蛋白27、促红细胞生成素、血红素加氧酶1对肾脏缺血再灌注损伤的影响**

背景：缺血再灌注损伤是临床导致急性肾衰竭等其他疾病的重要原因,其机制为多因素、多途径的复杂的病理过程。 目的：观察肾脏进行预处理后激活热休克蛋白、促红细胞生成素和血红素加氧酶1对肾脏缺血再灌注损伤的影响。 方法：雄性C57BL/6小鼠90只随机分成3组。缺血再灌注组为右肾切除,左肾缺血25 min再灌注24 h;预适应组为双侧肾脏缺血20 min再灌注8 d后再进行缺血再灌注。假手术组开腹游离肾蒂。 结果与结论：血清肌酐和尿素氮检测预适应组和假手术组明显低于缺血再灌注组(P < 0.01);MPO染色发现缺血再灌注组大量中性粒细胞浸润(P < 0.01);PAS染色发现预适应组肾组织病理情况轻于缺血再灌注组(P < 0.05);TUNEL染色分析结果表明预适应组和假手术组细胞凋亡数明显少于缺血再灌注组(P < 0.01);预适应组热休克蛋白27 mRNA表达明显高于缺血再灌注和假手术组(P < 0.05),热休克蛋白27 mRNA于第8天时最强,促红细胞生成素、血红素加氧酶1 mRNA在24~    48 h达到峰值A,然后逐渐下降,第8天后达到峰值B,B>A,并且高于假手术组(P < 0.01)。提示远期缺血预适应激活热休克蛋白27、促红细胞生成素、血红素加氧酶1,能减少炎症因子浸润、促进肾小管细胞修复和抑制细胞凋亡从而参与肾脏内源性保护机制。     

Effect of activation of the Ca2+-permeable acid-sensing ion channel 1a on focal cerebral ischemia in diabetic rats

We investigated the role of acid-sensing ion channel Ia (ASIC1a) expression and changes in intracellular Ca²⁺ concentration ([Ca²⁺]) in focal cerebral ischemia after middle cerebral artery occlusion (MCAO) in a rat model of diabetes mellitus (DM). Male Wistar rats (n = 108) were divided into three groups: the MCAO, DM + MCAO, and DM + MCAO + fasudil groups (n = 36 each). Samples were obtained 1, 3, 6, and 24 h after ischemia induction (n = 9). Rats in the DM + MCAO + fasudil group were treated with 1 mg/kg fasudil, a Rho-kinase inhibitor, by caudal vein injection 30 min after MCAO was performed. ASIC1a expression gradually increased with time in the MCAO and DM + MCAO groups (0.71 ± 0.10 nM, 0.80 ± 0.11 nM, 0.86 ± 0.08 nM, 0.93 ± 0.09 nM; 0.86 ± 0.11 nM, 1.05 ± 0.51 nM, 2.42 ± 0.08 nM, 2.78 ± 0.04 nM; pairwise comparisons at each time point, P < 0.05), and was higher in the DM + MCAO than the MCAO group (P < 0.05). [Ca²⁺] gradually increased in the DM + MCAO group (106.32 ± 18.6 nM, 137.84 ± 14.32 nM, 151.94 ± 18.38 nM, 183.61 ± 7.96 nM, P < 0.05). ASIC1a expression and calcium currents were reduced in the DM + MCAO + fasudil group. The overload of intracellular [Ca²⁺] caused by ASIC1a activation could be one mechanism for the aggravation of focal cerebral ischemia in diabetes.     

Ethyl pyruvate reduces hepatic mitochondrial swelling and dysfunction in a rat model of sepsis

Sepsis causes mitochondrial oxidative injury and swelling. Ethyl pyruvate (EP) is a cytoprotective agent, while aquaporin-8 (AQP8) is a mitochondrial water channel that can induce mitochondrial swelling. We assessed whether EP protects mitochondria during sepsis, and whether AQP8 contributes to the underlying mechanisms. A cecal ligation and puncture (CLP) sepsis model was established in Sprague-Dawley rats, randomized to 3 groups: sham (n=20), CLP (n=59) and CLP+EP (n=51). All rats received postoperative intraperitoneal fluid resuscitation (30 ml/kg); the CLP+EP group also received intraperitoneal EP (100 mg/kg). Survival was assessed at 24 hours. Hepatic mitochondrial ultrastructure was characterized by electron microscopy. The membrane potential of isolated hepatic mitochondria was determined using JC-1 and flow cytometry. Mitochondrial AQP8 expression and cytochrome C (Cyt C) release were measured by Western blotting (values normalized to ß-actin). Survival in the sham, CLP and CLP+EP groups was 100%, 21% and 41%, respectively. Mitochondrial cross-sectional area was smaller in the CLP+EP group than in the CLP group (0.231±0.110 vs. 0.641±0.460 µm²; P<0.001), with a tendency for a lower form factor (a measure of contour irregularity) in the CLP+EP group. Mitochondrial depolarization by CLP was inhibited by EP. Mitochondrial Cyt C release was higher in the CLP group than in the sham (1.211±0.24 vs. 0.48±0.03) or CLP+EP (0.35±0.39) groups. AQP8 expression was similar between groups, with a trend for lower expression in the CLP+EP group compared with the CLP group. EP improves sepsis outcome by targeting the mitochondrion, possibly through modulation of AQP8 expression.     

The regulation effect of ulinastatin on the expression of SSAT2 and AQP4 in myocardial tissue of rats after cardiopulmonary resuscitation

Objective: This study aims to investigate the regulation effects of ulinastatin (UT1) on the expression of spermidine/spermine -N1-acetyltransferase 2 (SSAT2) and aquaporin 4 (AQP4) in myocardial tissue of rats after cardiopulmonary resuscitation (CPR) and their correlations. Methods: A total of 90 adult SD rats were divided into sham operation group (A, n=30), model group (B, n=30) and UT1 group (C, n=30). The cardiac arrest (CA) and CPR model was established by asphyxia method. Left ventricular fractional shortening (LVFS), left ventricular ejection fraction (LVEF) and E/A peak ratio of mitral valve in three groups were collected by ultrasonic echocardiography. Apoptosis of myocardial cells was detected by DAPI staining. The expression levels of SSAT2 and AQP4 were detected by RT-PCR, Western blotting and immunohistochemical methods. Results: UT1 could significantly improve the levels of LVFS, LVEF and E/A ratio and decrease myocardial cell apoptosis. As compared with group B, the expression level of SSAT2 increased and the expression level of AQP4 decreased in group C (P<0.01). SSAT2 was the most in group A and the least in group B while AQP4 was the least in group A and the most in group B (P<0.01). There was positive correlation between SSAT2 and cardiac function in CRP model while there was negative correlation between AQP4 and cardiac function (P<0.01). The expression of SSAT2 and AQP4 protein in myocardial tissue was negatively correlated in CRP model (r=-0.920, P<0.01). Conclusions: UT1 can effectively reduce the cardiac function damage caused by CRP, which could be related with the increased SSAT2 and decreased AQP4.     

The Effect and Mechanism of Duodenal-Jejunal Bypass to Treat Type 2 Diabetes Mellitus in a Rat Model

ObjectivesBariatric surgery can treat obesity and T2DM, but the specific mechanism is unknown. This study investigated the effect and possible mechanism of duodenal-jejunal bypass (DJB) to treat T2DM.MethodsA T2DM rat model was established using a high-fat, high-sugar diet and a low dose of streptozotocin. DJB surgery and a sham operation (SO) were performed to analyze the effects on glucose homeostasis, lipid metabolism, and inflammation changes. Furthermore, the glucagon-like peptide-1 (GLP-1) in the ileum and the markers of endoplasmic reticulum stress (ERS) in the pancreas were examined after the surgery. The insulinoma cells (INS-1) were divided into three groups; group A was cultured with a normal sugar content (11.1 mmol/L), group B was cultured with fluctuating high glucose (11.1 mmol/L alternating with 33.3 mmol/L), and group C was cultured with fluctuating high glucose and exendin-4 (100 nmol/L). The cells were continuously cultured for 7 days in complete culture medium. The viability of the INS-1 cells was then investigated using the MTT method, apoptosis was detected by flow cytometry, and the ERS markers were detected by Western blot.ResultsThe blood glucose, lipids, insulin, and TNF-α were significantly elevated in the T2DM model. A gradual recovery was observed in the DJB group. GLP-1 expression in the distal ileum of the DJB group was significantly higher than that in the T2DM control group (DM) and the SO group (p < 0.05), and the markers of ERS expression in the pancreases of the DJB group decreased significantly more than those of groups DM and SO (p < 0.05). Compared with group A, the cell viability in group B was decreased, and the ERS and apoptosis were increased (p < 0.05). However, compared with group B, the cell viability in group C was improved, and the ERS and apoptosis declined (p < 0.05).ConclusionsDJB can be used to treat T2DM in T2DM rats. The mechanism may be that the DJB stimulates the increased expression of GLP-1 on the far side of the ileum, and then, GLP-1 inhibits ERS in the pancreas, reducing the apoptosis of β cells to create a treatment effect in the T2DM rats.