Effects of Microwave Exposure at Various Power Densities on Mitochondrial Marker Enzymes in Mouse Brains

Four groups of C₅₇BL mice were irradiated with 3 GHz pulse (PW) microwaves for 3 hours at incident power densities of 0.1, 0.5, 1 and 5 mW/cm² respectively. The amount of mitochondria1 marker enzymes succinate dehydrogenase (SDH) and monoamine oxidase (MAO) in the hypothalamus and hippocampus were determined by microspectrophotometry. SDH and MA0 in the irradiated groups (except 0.1 mW/cm²) were significantly lower compared to the control group (p < 0.01). The lowest level occurred in the 5 mW/cm² group. The threshold level was 0.5 mW/cm². To compare the effects of PW with continuous wave (CW) exposure, two experimental groups were exosed to 2.45 GHz, using CW; the enzymes were decreased only in the 5 mW/cm² group. The results show that PW radiation is more effective then CW radiation in decreasing SDH and MA0 levels.     

Lack of effect of 2.45-GHz microwave radiation on the development of preimplantation embryos of mice

The development of preimplantation embryos after exposure to microwave radiation was studied. Female CD-1 mice were induced to superovulate, mated, and exposed to 2.45-GHz microwave or sham radiation for 3 h at power densities of 9 mW/cm² and 19 mW/cm² on either day 2 or 3 of pregnancy (plug day was considered day 1). Another group of mice was exposed to heat stress by placing the dams in an environmental room at an ambient temperature of 38 °C and relative humidity at 62% for 3 h on day 2 of pregnancy. All groups were euthanized on day 4 of pregnancy and embryos were recovered by flushing excised uterine horns. Embryos were examined for abnormalities and classified by the developmental stages. They were then treated with hypotonic solution and dissociated for counting blastomeres. Heat stress caused stunted development of embryos, but no remarkable effect of microwave radiation could be found on the development of preimplantation embryos.     

Thymoquinone reduces mouse colon tumor cell invasion and inhibits tumor growth in murine colon cancer models

We have shown that thymoquinone (TQ) is a potent antitumor agent in human colorectal cancer cells. In this study, we evaluated TQ's therapeutic potential in two different mice colon cancer models [1,2-dimethyl hydrazine (DMH) and xenografts]. We also examined TQ effects on the growth of C26 mouse colorectal carcinoma spheroids and assessed tumor invasion in vitro. Mice were treated with saline, TQ, DMH, or combinations once per week for 30 weeks and the multiplicity, size and distribution of aberrant crypt foci (ACF) and tumors were determined at weeks 10, 20 and 30. TQ injected intraperitoneally (i.p.) significantly reduced the numbers and sizes of ACF at week 10; ACF numbers were reduced by 86%. Tumor multiplicity was reduced at week 20 from 17.8 in the DMH group to 4.2 in mice injected with TQ. This suppression was observed at week 30 and was long-term; tumors did not re-grow even when TQ injection was discontinued for 10 weeks. In a xenograft model of HCT116 colon cancer cells, TQ significantly (P < 0.05) delayed the growth of the tumor cells. Using a matrigel artificial basement membrane invasion assay, we demonstrated that sub-cyto-toxic doses of TQ (40 microM) decreased C26 cell invasion by 50% and suppressed growth in three-dimensional spheroids. Apoptotic signs seen morphologically were increased significantly in TQ-treated spheroids. TUNEL staining of xenografts and immunostaining for caspase 3 cleavage in DMH tumors confirmed increased apoptosis in mouse tumors in response to TQ. These data should encourage further in vivo testing and support the potential use of TQ as a therapeutic agent in human colorectal cancer.     

Chemopreventive efficacy of green tea drinking against 1,2‐dimethyl hydrazine‐induced rat colon carcinogenesis

Colorectal cancer is one of the leading causes of tumour‐related deaths. In the present study, the chemopreventive effect of green tea on 1,2‐dimethylhydrazine (DMH)‐induced colon carcinogenesis was studied in male Wistar rats. The DMH group received subcutaneous injections of DMH (30 mg kg^?1 body weight) once a week for 30 weeks, the normal group received the vehicle of DMH, and the DMH + green tea group received DMH simultaneously with 1% green tea as their sole source of drinking fluid throughout the experimental period. In the DMH group treated with green tea, significant reductions in gene overexpressions of colonic nuclear factor κB (NF‐κB), tumour necrosis factor α, inducible nitric oxide synthase and cyclooxygenase 2, and NF‐κB immunostaining indicates the anti‐inflammatory effect of green tea in attenuating colon cancer. Moreover, the anti‐angiogenic and anti‐invasiveness effects of green tea were revealed as reductions of both vascular endothelial growth factor and matrix metalloproteinase‐7 mRNA expression levels. These effects were confirmed by the significant reduction of serum tumour necrosis factor α, C‐reactive protein levels, inhibition of tumour incidence, and nearly normal survival rate and colonic architecture. It can be concluded that green tea exerts a potent chemopreventive effect on colon carcinogenesis possibly due to the inhibition of NF‐κB. Copyright © 2012 John Wiley & Sons, Ltd.     

Alteration of life span of mice chronically exposed to 2.45 GHz CW microwaves

Female CD 1 mice were exposed from the thirty-fifth day of age for the remainder of their lives to 2.45 GHz, CW-microwave radiation at a power density of 3 or 10 m W/cm² (SAR = 2.0 or 6.8 W/kg). Exposures took place 1 h/day, 5 day/week in an anechoic chamber at an ambient temperature of 22 °C and a relative humidity of 50%. There were 25 animals in each exposure group, and an equal number of controls were concurrently sham exposed. The average life span of animals exposed at 10 mW/cm² was significantly shorter than that of sham-exposed controls (572 days vs. 706 days; P = .049; truncation >20%). In contrast, the average lifespan of the animals exposed at 3 mW/cm² was slightly, but not significantly, longer (738 days) than that of controls (706 days). © 1994 Wiley-Liss, Inc.

1 This article is a US Government work and, as such, is in the public domain in the United States of America.

     

Effects of ovariectomy on microsatellite instability in rat colon tumors induced by 1,2-dimethylhydrazine

To study the effects of ovariectomy on tumorigenesis and microsatellite instability (MSI) in rat colon tumors induced by 1,2-dimethylhydrazine, to elucidate the association between postmenopausal ovarian hormones depletion and MSI pathway in colorectal tumorigenesis. Forty female Wistar rats were randomly divided into two groups: Ovariectomized (Ovx) group and Sham-ovariectomized (Sham-Ovx) group. All rats were injected intraperitoneally with 1,2-dimethylhydrazine (DMH) (20 mg/kg b.w) once a week for 20 weeks. Ten weeks after the final DMH injection, all the rats were sacrificed to collect tumors. Microsatellite instability of six microsatellite loci was detected using fluorescent PCR followed by fragment analysis on automatic DNA sequencer with GeneScan 3.7 software. The tumor multiplicity in the OVX group was significantly higher than that in the Sham-OVX group (3.6 ± 1.4 vs. 2.4 ± 1.6, P < 0.05). The incidence of MSI-positive tumors in OVX group was higher than that in Sham-OVX group (32.1 vs. 10.8%, P < 0.05).The incidence of tumors showing MSI at multiple loci in OVX group was also higher than that in Sham-OVX group (18.9 vs. 2.7%, P < 0.05). Ovariectomy increased tumor formation and the frequency of MSI in DMH-induced colon tumors. It implied that postmenopausal ovarian hormones depletion might influence colorectal tumorigenesis through MSI pathway.     

Inhibition of 1,2-dimethylhydrazine induced colon genotoxicity in rats by the administration of probiotic curd

Epidemiologic and experimental studies suggest that the probiotic organisms are effective in preventing colon carcinogenesis, which is the major cause of mortality and morbidity in western countries. Keeping this in view, a curd (a common Indian fermented milk product) was prepared by the addition of probiotic cultures Lactobacillus acidophilus, Lactobacillus casei and curd culture Lactococcus lactis biovar. diacetylactis. In present study, we have evaluated the anti tumor effect of probiotic curd by monitoring the DNA damage through comet assay. The rats were allocated to four groups, first group was DMH control group, second group was probiotic curd group in which probiotic curd was given along with DMH (1,2-dimethylhydrazine) injection, third group was normal curd group in which normal curd was given along with DMH injection and fourth group was normal control group. Animals received subcutaneous injection of DMH dissolved in normal saline at a dose rate of 20 mg/kg body weight, once weekly for 15 weeks. The rats were dissected at 40th week of experiment and comet assay was done in colonic cells to assess the DNA damage. A significant reduction in DNA damage (54.7%) was observed in probiotic curd group as compared to DMH control group (88.1%). The probiotic curd was effective to significantly reduce the L:W ratio in comparison to DMH control group and normal curd. The results of present study show the protective effects of probiotic curd against DMH induced genotoxicity in colonic cells.     

Vanadium inhibits placental glutathione S-transferase (GST-P) positive foci in 1,2-dimethyl hydrazine induced rat colon carcinogenesis

Vanadium (V) has recently been found to possess potent anti-neoplastic activity in rat colon carcinogenesis. In the present study attempts have been made to investigate the expression of the number and area of aberrant crypt foci positive for placental glutathione S-transferase (GST-P) during 1,2-dimethyl hydrazine (DMH)-induced rat colon carcinogenesis. Male Sprague Dawley rats were randomly divided into four groups. Rats in group A were designed as normal controls. Group B animals received DMH once a week (20 mg/kg body wt.) intraperitoneally for 16 weeks. Group C rats received the same treatment of DMH as in group B, along with 0.5-ppm vanadium as ammonium monovanadate ad libitum in drinking water throughout the experiment. Vanadium alone was given to Group D rats without any DMH injection. The expression of the number and the area of aberrant crypt foci (ACF) positive for GST-P was maximum in DMH-treated group. Vanadium-treated rats significantly reduced (P < 0.001) the expression of GST-P positive ACF cells (by 71.13%) for the entire period of the study. Moreover the histopathological examination also showed that vanadium action could minimize the aberrant crypt foci (P < 0.001). Furthermore, vanadium supplementation also elevated SOD activities in both liver and colon (P < 0.01, P < 0.02 and P < 0.01, P < 0.02 respectively) when compared to their carcinogen counterparts. Our results confirm that vanadium is particularly effective in limiting the action of the carcinogen, thereby establishing its anticarcinogenicity in chemically induced rat colon carcinogenesis.     

Effects of 2.45-GHz microwave radiation on embryonic quail hearts

Although exposure to nonionizing electromagnetic radiation has been reported to cause a variety of systemic alterations during embryonic development, there are few reports of the induction of specific physiologic or morphologic changes in the myocardium. This study was designed to examine the effects of microwave radiation on cardiogenesis in Japanese quail embryos exposed during the first eight days of development to 2.45-GHz continuous-wave microwaves at power densities of 5 or 20 mW/cm². The specific absorption rates were 4.0 and 16.2 mW/g, respectively. The ambient temperature for each exposure was set to maintain the embryonated eggs at 37.5 °C. This did not preclude thermal gradients in the irradiated embryos since microwaves may not be uniformly absorbed. The test exposure levels did not induce changes in either the morphology of the embryonic heart or the ultrastructure of the myocardial cells. Analysis of the enzymatic activities of lactate dehydrogenase, glutamic oxaloacetic transaminase, and creatine phosphokinase failed to reveal any statistically significant differences between the nonexposed controls and those groups exposed to either 5 or 20 mW/cm². The data indicate that 2.45-GHz microwave radiation at 5 or 20 mW/cm² has no effect on the measured variables of the Japanese quail myocardium exposed during the first eight days of development.     

Effects of microwave exposure and temperature on survival of mice infected with Streptococcus pneumoniae

Female CD-1 mice were injected with an LD₅₀ dose of Streptococcus pneumoniae and then exposed to 2.45 GHz (CW) microwave radiation at an incident power density of 10 mW/cm² (SAR = 6.8 W/kg), 4 h/d for 5 d at ambient temperatures of 19 °C, 22 °C, 25 °C, 28 °C, 31 °C, 34 °C, 37 °C and 40 °C. Four groups of 25 animals were exposed at each temperature with an equal number of animals concurrently sham-exposed. Survival was observed for a 10-d period after infection. Survival of the sham-exposed animals increased as ambient temperature increased from 19 °C–34 °C. At ambient temperatures at or above 37 °C the heat induced in the body exceeded the thermoregulatory capacity of the animals and deaths from hyperthermia occurred. Survival of the microwave-exposed animals was significantly greater than the shams (～20%) at each ambient temperature below 34 °C. Based on an analysis of the data it appears that the hyperthermia induced by microwave exposure may be more effective in increasing survival in infected mice than hyperthermia produced by conventional methods (ie, high ambient temperature). Microwave radiation may be beneficial to infected animals at low and moderate ambient temperatures, but it is detrimental when combined with high ambient temperatures.     

Accelerated development of spontaneous and benzopyrene-induced skin cancer in mice exposed to 2450-MHz microwave radiation

C₃H/HeA mice with high incidence of spontaneous breast cancer and Balb/c mice treated with 3,4-benzopyrene (BP) (by painting of the skin resulting in the development of skin cancer) were irradiated with 2,450-MHz microwaves (MW) in an anechoic chamber at 5 or 15 mW/cm² (2 h daily, 6 sessions per week). C₃H/HeA mice were irradiated from the 6th week of life, up to the 12th month of life. Balb/c mice treated with BP were irradiated either prior to (over 1 or 3 months) or simultaneously with BP treatment (over 5 months). The appearance of palpable tumors in C₃H/HeA mice and of skin cancer in BP-treated Balb/c mice was checked every 2 weeks for 12 months. Two additional groups of mice were exposed to chronic stress caused by confinement or to sham-irradiation in an anechoic chamber; these served as controls. Irradiation with MWs at either 5 or 15 mW/cm² for 3 months resulted in a significant lowering of natural antineoplastic resistance (mean number of lung neoplastic colonies was 2.8 ± 1.6 (SD) in controls, 6.1 ± 1.8 in mice exposed at 5 mW/cm² and 10.8 ± 2.1 in those irradiated at 15 mW/cm²) and acceleration of development of BP-induced skin cancer (285 days in controls, 230 days for 5 mW/cm² and 160 days for 15 mW/cm²). Microwave-exposed C₃H/HeA mice developed breast tumors earlier than controls (322 days in controls, 261 days for 5 mW/cm² and 219 days for 15 mW/cm²). A similar acceleration was observed in the development of BP-induced skin cancer in mice exposed simultaneously to BP and MWs (285 days in controls, 220 day for 5 mW/cm² and 121 days for 15 mW/cm²). The acceleration of cancer development in all tested systems and lowering of natural antineoplastic resistance was similar in mice exposed to MW at 5 mW/cm² or to chronic stress caused by confinement but differed significantly from the data obtained on animals exposed at 15 mW/cm², where local thermal effects (“hot” spots) were possible.     

Superoxide Dismutase Activity During Dimethylhydrazine Colon Carcinogenesis and the Effects of Cholic Acid and Indole

Copper, zinc superoxide dismutase (Cu, ZnSOD) and manganese superoxide dismutase (MnSOD) activities were measured in mouse large intestinal mucosa during dimethylhydrazine (DMH) carcinogenesis. Mice were divided into five groups. Group A was subcutaneously injected with DMH (20mg/kg) weekly and fed with a diet containing 0.2% cholic acid (C) and 0.8% indole (I). Group B was injected with DMH and given indole feeding. Group C was treated with DMH injection and cholic acid feeding. Group D was given DMH injection alone. Group E was an age-matched control group given 0.9% NaCl injection. The experiment last 21 weeks. The Cu, ZnSOD activity of intestinal mucosa in group A animals began to increase significantly at the 7th week of the experiment. In groups B, C and D, however, this enzyme was not elevated statistically until the 16th week, and then each of these groups kept an increased Cu, ZnSOD level the rest of the experimental period. MnSOD activity was elevated statistically in group C animals at the 7th week. The enzyme activity in group A and D animals increased at the 9th week, but the enzyme activity did not increase statistically until the 11th week in group B. After the 16th week of the experiment the increased activity of MnSOD in all experimental groups returned to the level of the control group. Large intestinal cancer tissues had increased Cu, ZnSOD activity and decreased MnSOD activity.     

Superoxide Dismutase Activity During Dimethylhydrazine Colon Carcinogenesis and the Effects of Cholic Acid and Indole

Copper, zinc superoxide dismutase (Cu, ZnSOD) and manganese superoxide dismutase (MnSOD) activities were measured in mouse large intestinal mucosa during dimethylhydrazine (DMH) carcinogenesis. Mice were divided into five groups. Group A was subcutaneously injected with DMH (20mg/kg) weekly and fed with a diet containing 0.2% cholic acid (C) and 0.8% indole (I). Group B was injected with DMH and given indole feeding. Group C was treated with DMH injection and cholic acid feeding. Group D was given DMH injection alone. Group E was an age-matched control group given 0.9% NaCl injection. The experiment last 21 weeks. The Cu, ZnSOD activity of intestinal mucosa in group A animals began to increase significantly at the 7th week of the experiment. In groups B, C and D, however, this enzyme was not elevated statistically until the 16th week, and then each of these groups kept an increased Cu, ZnSOD level the rest of the experimental period. MnSOD activity was elevated statistically in group C animals at the 7th week. The enzyme activity in group A and D animals increased at the 9th week, but the enzyme activity did not increase statistically until the 11th week in group B. After the 16th week of the experiment the increased activity of MnSOD in all experimental groups returned to the level of the control group. Large intestinal cancer tissues had increased Cu, ZnSOD activity and decreased MnSOD activity.     

Intervention of Acidophilus-casei dahi and Wheat bran against molecular alteration in colon carcinogenesis

An in vivo trial was conducted on seventy five rats allocated to three groups, first group was DMH control group, second group was Wheat bran-DMH group (WB-DMH) in which wheat bran was given along with DMH (1,2-dimethylhydrazine) injection, third group was Wheat bran-DMH-Ac Dahi group in which both wheat bran and Acidophilus-casei dahi (a probiotic microorganisms fermented dairy product) was given along with DMH injections. Animals received subcutaneous injections of DMH at a dose rate of 20 mg/kg body weight, once weekly for 15 weeks. The rats were dissected at 40th week of experiment and comet assay was done in colonic cells to assess the DNA damage. The c-myc and cox-2 expression was studied in rat tumour. A significant reduction in DNA damage (48.2%) was observed in WB-DMH-Ac Dahi group as compared to DMH control group (87.8%). The c-myc and cox-2 mRNA level was found highest in DMH control group as compared to WB-DMH and WB-DMH-Ac Dahi group. The results of present study show the enhanced protective potential of Acidophilus-casei and wheat bran against DMH induced molecular alteration in colonic cells during carcinogenesis.     

Changes in the Intestinal Microflora in Association with Colon Tumorigenesis in Rats Treated with 1,2-Dimethylhydrazine Hydrochloride

The present study was undertaken to determine whether the intestinal microflora change during the tumorigenic process in the colon of rats treated with 1,2-dimethylhydrazone (DMH), and to compare the intestinal microflora of rats with colon tumors induced by DMH with that of rats with gastric tumors induced by N-methyl-N′-nitro-N-nitrosoguanidine (MNNG). When compared with those in the control animals, the numbers of streptococci and bacteroidaceae were moderately increased in the intestinal tract of DMH-treated rats before the development of visible intestinal tumors. The DMH-treated rats bearing small intestinal and colonic tumors were found to have markedly increased numbers of enterobacteriaceae, Clostridium perfringens, streptococci, bacteroidaceae, and bifidobacteria. In DMH-induction the overgrowth of enterobacteriaceae and/or C. perfringens was found to correlate with the size and number of tumors in both the small intestine and colon. The increased number of streptococci in the DMH-treated rats was principally due to an increase in the number of the streptococci which did not reduce triphenyltetrazolium chloride (TTC). On the other hand, in the rats with gastric tumors induced by MNNG the numbers of enterobacteriaceae and TTC-reducing streptococci were remarkably increased in the intestinal tract of only the debilitated animals, and Pseudomonas aeruginosa was detected in all of them. The number of anaerobic gram-positive cocci was significantly but not remarkably increased in the gastric tumor-bearing rats compared with the controls. These results indicate that the intestinal microflora of rats may change depending on the gastrointestinal site where tumors develop and the degree of malignancy in tumorigenesis.     

Chemoprevention of lung cancer by lycopene

An investigation was conducted to assess the chemopreventive potential of lycopene (LP), a naturally occurring hydrocarbon carotenoid found in tomatoes and their products, administered during the post-initiation stage in a multiorgan carcinogenesis model. One hundred eighteen B6C3F1 mice of both sexes were subjected to combined treatment with diethylnitrosamine (DEN), N-methyl-N-nitrosourea (MNU) and 1,2-dimethylhydrazine (DMH) from day 11 after birth to week 9 (DMD treatment) (groups 1 and 2) or given their vehicles (group 3). Then group 1 received LP (25 or 50 ppm in drinking water) for 21 weeks from weeks 11 to 32. Group 2 served as a carcinogen alone control and group 3 was given only LP (25 or 50 ppm). The incidences and multiplicities of lung adenomas plus carcinomas combined in male mice in group 1 receiving LP 50 ppm were significantly decreased as compared to the DMD alone or DMD and LP 25 ppm group values (75.0 vs 18.8%, P < 0.02; 0.94+/-0.17 v.s 0.25+/-0.14, P < 0.001). While hepatocellular carcinomas were lacking in the DMD and LP groups, two cases were found in the DMD alone group (not statistically significant). The values for aberrant crypt foci (ACF) and tumors in the colon and kidney did not show any significant variation among the carcinogen-treated subgroups. The results of this study provide evidence that the tomato carotenoid, lycopene, may have potential as a chemopreventive agent against carcinogenesis in the male lung.     

鼠衣原体改善DSS诱导的小鼠溃疡性结肠炎的作用研究

【目的】探讨鼠衣原体(Chlamydia muridarum)对小鼠溃疡性结肠炎的作用。【方法】取15只雌性C57BL/6J小鼠随机分为3组,每组5只动物,分别为空白对照组(Control)、肠炎模型组(DSS)、实验组(CM+DSS)。选取CM+DSS组小鼠予以2×10⁵ IFU的鼠衣原体灌胃处理,并在其感染后第29天开始,给予DSS组和CM+DSS组的小鼠2%DSS饮水,持续5d,每天监测小鼠体重和肠炎疾病评分,实验结束后检测小鼠结肠长度和结肠组织炎性改变。【结果】肠炎模型组的小鼠均表现出典型的肠炎症状(包括体重减轻、肠炎疾病评分、结肠长度和组织炎性改变);而经鼠衣原体预处理的小鼠(CM+DSS组)肠炎症状显著减轻,表现在肠炎疾病评分降低,体重和结肠长度有所恢复,肠组织炎性损伤减轻。【结论】鼠衣原体对DSS诱导的小鼠溃疡性结肠炎具有改善作用。     

Effects of Selenium and L-Carnitine on Oxidative Stress in Blood of Rat Induced by 2.45-GHz Radiation from Wireless Devices

The levels of blood lipid peroxidation, glutathione peroxidase, reduced glutathione, and vitamin C were used to follow the level of oxidative damage caused by 2.45 GHz electromagnetic radiation in rats. The possible protective effects of selenium and L-carnitine were also tested and compared to untreated controls. Thirty male Wistar Albino rats were equally divided into five groups, namely Groups A₁ and A₂: controls and sham controls, respectively; Group B: EMR; Group C: EMR + selenium, Group D: EMR + L-carnitine. Groups B–D were exposed to 2.45 GHz electromagnetic radiation during 60 min/day for 28 days. The lipid peroxidation levels in plasma and erythrocytes were significantly higher in group B than in groups A₁ and A₂ (p?<?0.05), although the reduced glutathione and glutathione peroxidase values were slightly lower in erythrocytes of group B compared to groups A₁ and A₂. The plasma lipid peroxidation level in group A₂ was significantly lower than in group B (p?<?0.05). Erythrocyte reduced glutathione levels (p?<?0.01) in group B; erythrocyte glutathione peroxidase activity in group A₂ (p?<?0.05), group B (p?<?0.001), and group C (p?<?0.05) were found to be lower than in group D. In conclusion, 2.45 GHz electromagnetic radiation caused oxidative stress in blood of rat. L-carnitine seems to have protective effects on the 2.45-GHz-induced blood toxicity by inhibiting free radical supporting antioxidant redox system although selenium has no effect on the investigated values.     

粪肠球菌MG 2108对小鼠结肠炎症的缓解作用及机制研究

【目的】为了筛选能抑制鼠类柠檬酸杆菌(Citrobacter rodentium)诱发的小鼠结肠炎的益生菌,并研究其干预机制。【方法】对4株筛选的菌株进行人工模拟胃肠液耐受试验,并体外测试它们对鼠类柠檬酸杆菌的抑制能力,最终筛选出粪肠球菌(Enterococcus faecalis)MG 2108。72只雄性7周龄ICR小鼠经过适应性饲养7d后,被随机分为2组：正常对照组(MC组,24只,生理盐水)和炎症对照组(IC组,48只,1×10¹⁰CFU/mL灌胃鼠类柠檬酸杆菌),7d后各采12只小鼠,通过结肠组织HE染色和炎症因子检测实验,判断炎症模型建成。原MC组(剩下12只小鼠)更名为NC组,用以区别建模前后的正常对照组,IC组随机分成3组：自然恢复组(IR组,12只,生理盐水)、环丙沙星组(CF组,12只,4mg/mL环丙沙星)和粪肠球菌MG 2108组(EF组,12只,1×10⁸CFU/mL粪肠球菌MG 2108)。18d后结束灌胃,所有小鼠麻醉后眼球取血,解剖。【结果】粪肠球菌MG 2108可以缓解和修复鼠类柠檬酸杆菌引发的小鼠结肠和肝脏损伤,并且通过降低炎症细胞因子的表达水平和增加紧密连接蛋白的表达水平,促进了结肠炎症组织的修复。它改变了肠道微生物菌群结构,EF组的肠杆菌属(Enterorhabdus)和阿克曼菌属(Akkermansia)等有益菌群的丰度增加,同时短链脂肪酸也显著增加(P<0.05),并且优于CF组和IR组。【结论】粪肠球菌MG2108是一株有利于肠道健康的益生菌,治疗鼠类柠檬酸杆菌诱导的小鼠结肠炎效果优于环丙沙星,自然恢复组效果明显差于EF组。     

Adiponectin deficiency: role in chronic inflammation induced colon cancer

Adiponectin (APN), an adipokine, exerts an anti-inflammatory and anti-cancerous activity with its role in glucose and lipid metabolism and its absence related to several obesity related malignancies including colorectal cancer. The aim of this study is to determine the effect of APN deficiency on the chronic inflammation-induced colon cancer. This was achieved by inducing inflammation and colon cancer in both APN knockout (KO) and C57B1/6 wild type (WT) mice. They were divided into four treatment groups (n=6): 1) control (no treatment); 2) treatment with three cycles of dextran sodium sulfate (DSS); 3) weekly doses of 1,2-dimethylhydrazine (DMH) (20mg/kg of mouse body weight) for twelve weeks; 4) a single dose of DMH followed by 3 cycles of DSS (DMH+DSS). Mice were observed for diarrhea, stool hemoccult, and weight loss and were sacrificed on day 153. Tumor area and number were counted. Colonic tissues were collected for Western blot and immunohistochemistry analyses. APNKO mice were more protected than WT mice from DSS induced colitis during first DSS cycle, but lost this protection during the second and the third DSS cycles. APNKO mice had significantly severe symptoms and showed greater number and larger area of tumors with higher immune cell infiltration and inflammation than WT mice. This result was further confirmed by proteomic study including pSTAT3, pAMPK and Cox-2 by western blot and Immunohistochemistry. Conclusively, APN deficiency contributes to inflammation-induced colon cancer. Hence, APN may play an important role in colorectal cancer prevention by modulating genes involved in chronic inflammation and tumorigenesis.