OBJECTIVETo investigate the expression of 17 beta-hydroxysteroid dehydrogenase type 1 (17β-HSD1) in the kidney of rats and explore the capacity of the kidney for synthesizing sex hormones.

METHODSThe expressions of 17-HSD1 and sex hormones were detected by Western blotting and radioimmunoassay in rat renal cells in primary cultured for 24 and 48 h in the presence or absence of follicle-stimulating hormone (FSH) and luteinizing hormone (LH).

RESULTSAfter cell culture for 24 h, the primary rat renal cells expressed a low level of 17β-HSD1 (0.1843±0.076), which increased to 1.6651±0.044 (P<0.01) in response to co-stimulation by FSH and LH. Low levels of estradiol, progesterone and testosterone were also detected in rat renal cells (3.30±3.78, 62.60±12.33, and 22.12±3.36, respectively), and co-stimulation of FSH and LH significantly increased their levels to 8.50±2.64, 117.80±9.79, and 45.04±4.39, respectively (P<0.05). The levels of these hormones showed no significant differences between cells cultured for 24 h and 48 h (P>0.05).

CONCLUSIONThe rat renal cells express 17β-HSD1 and are capable of stably secreting sex hormones in response to co-stimulation with FSH and LH, suggesting the capacity of the rat kidneys for synthesizing sex hormones. These findings enrich the understanding of the endocrine function of the kidney.

17-Hydroxysteroid Dehydrogenases ; metabolism ; Animals ; Cells, Cultured ; Estradiol ; biosynthesis ; Follicle Stimulating Hormone ; pharmacology ; Kidney ; enzymology ; Luteinizing Hormone ; pharmacology ; Progesterone ; biosynthesis ; Rats ; Testosterone ; biosynthesis

OBJECTIVETo determine the physiological role of D-bifunctional protein (DBP) in bile acid biosynthesis through investigating the effect of increasing activity of DBP on bile acid biosynthesis.

METHODSTwenty male Wistar rats were divided into two groups: diethylhexyl phthalate (DEHP) group (n = 10) and control group (n = 10). Serum triglyceride, total cholesterol, hepatic DBP activity, and fecal bile acids were assayed. The mRNA levels of hepatic peroxisome proliferator-activated receptor alpha (PPARalpha), DBP, and cholesterol 7alpha-hydroxylase (CYP7A1) were detected by RT-PCR.

RESULTSCompared with control group, serum triglyceride level was decreased significantly and PPARalphamRNA level was increased significantly in DEHP group (P < 0.01). Together with a sharp induction of DBP mRNA expression and DBP activity in DEHP group (P < 0.01), the levels of CYP7A1 mRNA and fecal bile acids were significantly increased by 1.9 times and 1.6 times respectively compared to control group (P < 0.01). There was a significantly positive correlation between DBP mRNA level or DBP activity and CYP7A1 mRNA level (r = 0.89, P < 0.01; r = 0.95, P < 0.01).

CONCLUSIONThe up-regulation of DBP mRNA and activity in liver can result in the increase in CYP7A1 mRNA expression and bile acid biosynthesis, suggesting that DBP may be involved in bile acid biosynthesis together with CYP7A1.

17-Hydroxysteroid Dehydrogenases ; metabolism ; Animals ; Bile Acids and Salts ; biosynthesis ; Cholesterol 7-alpha-Hydroxylase ; analysis ; Enoyl-CoA Hydratase ; metabolism ; Liver ; metabolism ; Male ; Multienzyme Complexes ; metabolism ; PPAR alpha ; analysis ; Peroxisomal Multifunctional Protein-2 ; RNA, Messenger ; analysis ; Random Allocation ; Rats ; Rats, Wistar

OBJECTIVETo evaluate the inhibitory effect of genistin combined with anastrozole on the growth and apoptosis of breast tumor tissue, and to study their anti-cancer mechanism by using the model of 7,12-dimethylbenz [alpha] anthracene (DMBA)-induced mammary tumors following ovariectomy in Sprague-Dawley (SD) rats.

METHODSThe DMBA induced postmenopausal SD rats were randomly divided into the control group, the genistein group, the anastrozole group, and the genistein combined with anastrozole group. The growth of tumors was observed in each group. The proliferation index and apoptosis index of tumor cells were determined. Moreover, estradiol (E2) and 17beta-HSD1 mRNA levels were determined by ELISA and RT-PCR respectively.

RESULTSThe tumor growth was inhibited in the genistein group and the anastrozole group. The inhibitory ratio was significantly higher in the genistein combined with anastrozole group (P < 0.05). Compared with the control group, levels of E2 and 17beta-HSD1 mRNA decreased more significantly in the genistein combined with anastrozole group (P < 0.05).

CONCLUSIONSGenistein could suppress the growth of mammary tumors in postmenopausal rats. It showed synergistic effect when combined with anastrozole, which resulted in reduced levels of E2 and 17beta-HSD1 mRNA. It had inhibitory effect on the growth of breast tumors.

17-Hydroxysteroid Dehydrogenases ; metabolism ; Animals ; Cell Line, Tumor ; Cell Proliferation ; drug effects ; Estradiol ; metabolism ; Female ; Genistein ; administration & dosage ; pharmacology ; Mammary Neoplasms, Experimental ; chemically induced ; pathology ; Nitriles ; administration & dosage ; pharmacology ; Ovariectomy ; Postmenopause ; Rats ; Rats, Sprague-Dawley ; Triazoles ; administration & dosage ; pharmacology

OBJECTIVETo explore the mechanism of inhibitory effect of SLW on estrogen production by endometrial cells of endometriosis.

METHODAfter the model of eutopic primary cultured endometrial cells of endometiosis and hysteromyoma in vitro was successfully established, the changes of steroidgenic factor-1 (SF-1), chicken ovalbumin upstream-transcription factor (COUP-TF), 17-beta-hydroxysteroid dehydrogenase 1 (17-beta-HSD1) and 17-beta-hydroxysteroid dehydrogenase 2 (17-beta-HSD2) mRNA were detected by RT-PCR before and after treatment of medicated serum of SLW. The changes of SF-1 and COUP-TF protein were also observed by western blot synchronously according to the same treatment method mentioned-above. Meanwhile ,the data of hysteromyoma group was obtained from the above experiments.

RESULTThe expression of SF-1 mRNA and protein, 17-beta-HSD1 mRNA was weak, but COUP-TF mRNA and protein, 17-beta-HSD2 mRNA was remarkable in Hysteromyoma endometrium, as compared with those of endometiosis ,which was taken as control group (P<0.01). After the 48 hours' treatment of medicated serum of 5.0, 2.5 g kg(-1) d(-1) of SLW , the expression of COUP-TF mRNA and protein, 17beta-HSD2 mRNA was found significantly increased, but SF-1 mRNA and protein, 17-beta-HSD 1 mRNA was decreased in contrast to the control group (P <0.01 or P <0.05). Although the expresson of COUP-TF mRNA and protein was increased, SF-1 protein and 17-beta-HSD1 mRNA was decreased in 1.25 g kg(-1) d(-1) medicated serum group ,compared with those of the control group (P <0.01), the low dose group had no apparent inhibitory effect on the expression of SF-1, 17-beta-HSD2 mRNA.

CONCLUSIONThe medicated serum of SLW could inhibit the secretion of estradiol in eutopic endometrial cells of endometiosis, and its mechanism might be associated with combined action of inhibiting expression of SF-1, 17-beta-HSD1 and up-regulating expression of COUP-TF, 17-beta-HSD2.

17-Hydroxysteroid Dehydrogenases ; genetics ; Adult ; Animals ; COUP Transcription Factors ; genetics ; Drugs, Chinese Herbal ; pharmacology ; Endometriosis ; blood ; metabolism ; pathology ; Endometrium ; drug effects ; metabolism ; pathology ; Estradiol Dehydrogenases ; Estrogens ; biosynthesis ; Female ; Gene Expression Regulation ; drug effects ; Humans ; In Vitro Techniques ; Middle Aged ; RNA, Messenger ; genetics ; metabolism ; Rats ; Serum ; chemistry ; Steroidogenic Factor 1 ; genetics

OBJECTIVETo investigate the alteration of the gene HSD17B4 in esophageal squamous cell carcinoma and its potential significance.

METHODSThe mRNA expression and loss of heterozygosity (LOH) of HSD17B4 in 40 primary esophageal tumors were detected by reverse transcriptase-polymerase chain reaction (RT-PCR) and microsatellite analysis with the intragenic marker D5S1384 of the gene.

RESULTSThe frequencies of allelic loss of D5S1384 and the rate of down-regulation of gene HSD17B4 were 46.2% and 62.5%, respectively.

CONCLUSIONHSD17B4 may be a candidate tumor suppressor gene associated with esophageal squamous cell carcinoma.

17-Hydroxysteroid Dehydrogenases ; biosynthesis ; genetics ; Adult ; Aged ; Carcinoma, Squamous Cell ; genetics ; Down-Regulation ; Enoyl-CoA Hydratase ; biosynthesis ; genetics ; Esophageal Neoplasms ; genetics ; Female ; Gene Expression ; Gene Expression Regulation, Neoplastic ; genetics ; Genes, Tumor Suppressor ; Humans ; Hydro-Lyases ; Loss of Heterozygosity ; Male ; Microsatellite Repeats ; Middle Aged ; Multienzyme Complexes ; biosynthesis ; genetics ; Peroxisomal Multifunctional Protein-2 ; RNA, Messenger ; biosynthesis ; genetics ; Reverse Transcriptase Polymerase Chain Reaction

OBJECTIVE: To explore the genetic basis for a sib pair featuring 17beta-hydroxysteroid dehydrogenase type 3 deficiency. METHODS: Genomic DNA was extracted from the proband, her sister, and their parents, and was subjected to sequencing analysis with a gene panel for sexual development. Suspected variant was verified by Sanger sequencing and bioinformatic analysis. RESULTS: Both the proband and her sister were found to harbor novel compound heterozygous missense variants of the HSD17B3 gene, namely c.839T>C (p.Leu280Pro) and c.239G>T (p.Arg80Leu), which were derived respectively from their mother and father. The variants were unreported previously and predicted to be deleterious by PolyPhen2, MutationTaster and other online software. Based on the American College of Medical Genetics and Genomics standards and guidelines, both c.839T>C(p.Leu280Pro) and c.239G>T (p.Arg80Leu) were predicted to be likely pathogenic (PM2+PP1+PP2+PP3+PP4, PM2+PM5+PP1+PP2+PP3+PP4). CONCLUSION The compound heterogeneous variants of the HSD17B3 gene probably underlay the disease in this sib pair. 17beta-hydroxysteroid dehydrogenase type 3 deficiency may lack specific clinical features and laboratory index, genetic testing can facilitate a definitive diagnosis.
17-Hydroxysteroid Dehydrogenases/genetics* ; Female ; Genetic Testing ; Genomics ; Humans ; Mutation ; Mutation, Missense

BACKGROUND: Diabetes is characterized by chronic hyperglycemia, and hyperglycemia can increase reactive oxygen species (ROS) production from the mitochondrial electron transport chain. The formation of ROS in cells induces oxidative stress and activates oxidative damage-inducing genes. There is no research on the protein levels of oxidative damage-related genes AKR1C3 in human diabetic skin. We explored the expression of AKR1C3 in diabetic skin compared with normal skin tissue. OBJECTIVE: To compare the expression of AKR1C3 in normal skin versus diabetic skin. METHODS: AKR1C3 expression was evaluated by western blotting in 6 diabetic skin tissue samples and 6 normal skin samples. Immunohistochemical staining was carried out to analyze AKR1C3 expression in the 6 diabetic skin tissue samples (July 2009 to December 2011; Department of Plastic and Reconstructive Surgery at Soonchunhyang University Seoul Hospital, Seoul, Korea). RESULTS: The western blotting showed a significant reduction in AKR1C3 protein expression in diabetic skin tissue compared to normal tissue. Immunohistochemical examination of AKR1C3 showed that it was weakly expressed in all diabetic skin samples. CONCLUSION: We believe that AKR1C3 is related to diabetic skin in altered metabolic states which elevate ROS production.
17-Hydroxysteroid Dehydrogenases ; Blotting, Western ; Electron Transport ; Humans* ; Hyperglycemia ; Oxidative Stress ; Oxidoreductases* ; Plastics ; Reactive Oxygen Species ; Skin*

The aim of the present study was to investigate the expression changes of three steroidogenic enzymes in the polycystic ovary syndrome (PCOS). Thirty Sprague-Dawley (SD) rats were randomly divided into normal control (NC) group and PCOS group. PCOS rat model was established by DHEA injection. The serum levels of progesterone, estrogen and testosterone were measured by immunoradioassay or enzyme immunoassay. The cellular distributions of 3β-hydroxy steroid dehydrogenase (3β-HSD), 17β-hydroxy steroid dehydrogenase (17β-HSD) and cytochrome P450 aromatase (P450arom) in ovaries were detected by immunohistochemistry. The expression levels of 3β-HSD, 17β-HSD and P450arom were detected by RT-PCR and Western blot. The results showed that the serum levels of estrogen and testosterone of PCOS group were significantly higher than those of the NC group. There was no significant difference of serum progesterone level between the PCOS and NC groups. Compared with the NC group, the PCOS group showed increased mRNA and protein expressions of both 3β-HSD and 17β-HSD, as well as reduced P450arom mRNA and protein expressions. These results suggest that 3β-HSD and 17β-HSD, but not P450arom, may participate in the ovarian hormonal regulation in the present rat model of PCOS.
17-Hydroxysteroid Dehydrogenases ; metabolism ; 3-Hydroxysteroid Dehydrogenases ; metabolism ; Animals ; Aromatase ; metabolism ; Disease Models, Animal ; Estrogens ; blood ; Female ; Polycystic Ovary Syndrome ; enzymology ; Progesterone ; blood ; Rats ; Rats, Sprague-Dawley ; Testosterone ; blood

OBJECTIVETo explore the biological effects of infrasound on the polygonal cells in adrenal cortex zona fasciculation in mice.

METHODSThe biological effects of infrasound on the activities of 3beta hydroxysteroid dehydrogenase (3-betaHSDH) and acid phosphatase(ACP) of the polygonal cells in adrenal cortex zona fasciculate were observed when exposure to 8 and 16 Hz infrasound at 80, 90, 100, 110, 120 and 130 dB for 1 day, 7 days and 14 days or 14 days after the exposure.

RESULTSWhen exposure to 8 Hz infrasound, the enzyme activities of 3-betaHSDH increase as the sound pressure levels increase. Only when the sound pressure levels reach 130 dB, the enzyme activities began to decrease exceptionally. When exposure to 16 Hz, 80 dB infrasound, no significant difference between the treatment and control group in the activities of 3-betaHSDH could be observed, but the injury of the polygonal cells had appeared. When exposure to 16 Hz, 100 dB infrasound, the activities of 3-betaHSDH started to increase. The cell injury still existed. When exposed to 16 Hz, 120 dB infrasound, the local tissue damage represented. Fourteen days after the mice exposure to 8 Hz, 90 dB and 130 dB infrasound for 14 days continuously, the local tissue injury of the adrenal cortex zona fasciculation began to recover at certain extent, but the higher the exposure sound pressure level, the poorer the tissue recovery.

CONCLUSIONThe biological effects of infrasound on the polygonal cells in adrenal cortex zona fasciculation response to the frequency of the infrasound are found at certain action strength range, but this characteristic usually is covered by the severe tissue injury. When exposure to infrasound is stopped for a period of time, the local tissue injury of the adrenal cortex zona fasciculation could recovers at certain extent, but the higher the exposure sound pressure level, the more poorer the tissue recovery.

17-Hydroxysteroid Dehydrogenases ; metabolism ; Acid Phosphatase ; metabolism ; Adrenal Cortex ; cytology ; enzymology ; Animals ; Environmental Exposure ; Male ; Mice ; Mice, Inbred BALB C ; Noise ; Zona Fasciculata ; enzymology ; Zona Reticularis ; enzymology

Non-alcoholic fatty liver disease (NAFLD) is an epidemic metabolic condition driven by an underlying lipid homeostasis disorder. The lipid droplet (LD), the main organelle involved in neutral lipid storage and hydrolysis, is a potential target for NAFLD therapeutic treatment. In this review, we summarize recent progress elucidating the connections between LD-associated proteins and NAFLD found by genome-wide association studies (GWAS), genomic and proteomic studies. Finally, we discuss a possible mechanism by which the protein 17β-hydroxysteroid dehydrogenase 13 (17β-HSD13) may promote the development of NAFLD.
17-Hydroxysteroid Dehydrogenases ; genetics ; metabolism ; Animals ; Genome-Wide Association Study ; Genomics ; Humans ; Lipid Droplets ; metabolism ; Lipid Metabolism ; genetics ; Non-alcoholic Fatty Liver Disease ; genetics ; metabolism ; Proteomics