OBJECTIVETo investigate the role of the extracellular signal-regulated protein kinase 1/2 (ERK1/2) pathway in erectile dysfunction (ED) caused by the absence of testosterone (T).

METHODSWe randomly divided 30 eight-week-old healthy male SD rats into groups A (control) , B (castration), and C (castration + androgen replacement). The rats in groups B and C were castrated surgically, and those in C injected with T undecanoate (100 mg/kg) at 1 week after castration, while the others with 0.9% normal saline instead. At 1 month after treatment, we determined the serum T level, intracavernous pressure (ICP), and mean carotid arterial pressure (MAP) of the rats, and detected the expressions of ERK1/2 and endothelial nitric oxide synthase (eNOS) by Western blot.

RESULTSThe serum T level was significantly lower in group B ([1.27 ± 0.48] nmol/L) than in A ([17.14 ± 1.07] nmol/L) and C ([16.24 ± 1.90] nmol/L) (P < 0.05), and so were ICP and MAP (P < 0.05). The expression of ERK1/2 showed no statistically significant differences among the three groups (P > 0.05), that of phosphatase ERK1/2 was markedly higher while that of eNOS remarkably lower in group B than in A and C (both P < 0.05).

CONCLUSIONAndrogen replacement may improve the erectile function of castrated rats by regulating the ERK1/2 pathway.

Androgens ; therapeutic use ; Animals ; Blotting, Western ; Erectile Dysfunction ; drug therapy ; metabolism ; Hormone Replacement Therapy ; MAP Kinase Signaling System ; Male ; Mitogen-Activated Protein Kinase 1 ; metabolism ; Mitogen-Activated Protein Kinase 3 ; metabolism ; Nitric Oxide Synthase Type III ; metabolism ; Orchiectomy ; Penile Erection ; Penis ; Rats ; Rats, Sprague-Dawley ; Testosterone ; analogs & derivatives ; therapeutic use

Three sesquiterpenoids and nine iridoids were isolated from the roots and rhizomes of Valeriana jatamansi by various chromatographic methods. Their structures were identified by physicochemical properties, NMR and MS data. Among them, valeriananoid G (1) was a new patchoulol-type sesquiterpenoid, and compound 3 was isolated from the genus Valeriana for the first time. Compounds 3 and 10 exhibited significant inhibitory effects on nitric oxide production induced by lipopolysaccharide in RAW 264.7 macrophages, with IC₅₀ values of 19.00 and 3.66 μmol·L^-1, respectively. In addition, compounds 4, 6 and 12 showed anti-influenza virus activity with IC₅₀ values of 51.75, 51.40 and 102.08 μmol·L^-1, respectively.

Objective:To investigate the expression and diagnostic value of SS18-SSX fusion-specific antibody and SSX C-terminal antibody in synovial sarcoma (SS).Methods:Immunohistochemical (IHC) EnVision method was used to detect the expression of SS18-SSX fusion-specific antibody and SSX C-terminal antibody in 51 genetically confirmed cases of SS and 94 non-SS tumors diagnosed at Nanjing Jinling Hospital from August 2013 to December 2020.Results:IHC staining for SS18-SSX fusion-specific antibody revealed strongly diffuse nuclear staining in 48 of 51 (48/51, 94.1%) SS cases, whereas none of the 94 non-SS tumors showed any staining. IHC staining for SSX C-terminal antibody showed strongly diffuse nuclear staining in all 51 (51/51, 100%) SS cases; six of the 94 (6/94, 6.4%) non-SS tumors showed variable staining, including two cases each of leiomyosarcoma and fibrosarcoma, and one case each of malignant peripheral nerve sheath tumor and embryonal rhabdomyosarcoma. The sensitivity and specificity of SS18-SSX fusion-specific antibody in diagnosing SS were 94.1% and 100% and these of SSX C-terminal antibody were 100% and 93.6%, respectively.Conclusions:SS18-SSX fusion-specific antibody and SSX C-terminal antibody are highly sensitive and specific markers for SS. Immunohistochemistry using these antibodies may replace FISH or molecular genetic testing in most cases.

Aim To study the anti-inflammatory activ¬ity of diterpenes from Tripterygium wilfordii on lipopo- lysaccharide ( LPS)-induced macrophage and its mech¬anism. Methods MTT assay was used to detect the cytotoxicity of compounds. The Griess method was used to detect the NO on LPS-induced RAW264. 7 cells. ELISA was applied to determine the contents of inter- leukin 6 (IL-6) , tumor necrosis factor a ( TNF-a ) , interleukin lp (IL-lfj) and interleukin 18 (IL-18) in cell culture supernatant. Western blot was used to de¬tect IkBcx, .INK, ERK, p38, STAT3 and their phos-phorylation in LPS-induced RAW264.7, as well as the effect on COX-2, iNOS, NLRP3, caspase-1 , cleaved- caspase-1. Flow cytometry was employed to detect the effects of compounds on the phagocytosis of RAW 264. 7 cells. Results Hypoglicin II (1) and ent-pimara-8 (14) , 15-diene-19-ol (6) , two diterpenoid compounds from Tripterygium wilfordii could effectively inhibit the expression of inflammatory mediators ( COX-2 and iN- OS) and inflammatory cytokines (IL-6, IL-lp, IL- 18) in LPS-induced RAW264. 7 cells. Further re¬search found that the phosphorylation of IkBcx , JNK, ERK, P38, STAT3 and NLRP3 was all inhibited; however, there was no significant effect on the expres¬sion of IkBcx, JNK, ERK, P38 and STAT3. At the same time, they also inhibited the phagocytosis of mac-rophages. Conclusions The anti-inflammatory mecha¬nism of Tripterygium wilfordii diterpenoids 1 and 6 might be through inhibiting the production of NLRP3 inflammatory bodies, inflammatory mediators (COX-2 and iNOS) and inflammatory cytokines (IL-6, IL-lp and IL-18) , which is closely related to inhibiting the activation of MAPK, NF-kB and STAT3 pathway.

Fourteen new geranyl phenyl ethers (1-14) along with three known compounds (15-17) were isolated from Illicium micranthum, and their structures were elucidated by comprehensive spectroscopic methods. Illimicranins A-H (1-8) were characterized as geranyl vanillin ethers, while 9 and 10 were dimethyl acetal derivatives. Illimicranins I and J (11 and 12) were rare geranyl isoeugenol ethers. Illimicranins K and L (13 and 14) represented the first example of geranyl guaiacylacetone ether and geranyl zingerone ether, respectively. Compounds 1, 2 and 15 exhibited anti-HBV (hepatitis B virus) activity against HBsAg (hepatitis B surface antigen) and HBeAg (hepatitis B e antigen) secretion, and HBV DNA replication.
Antiviral Agents/pharmacology* ; Hepatitis B Surface Antigens ; Hepatitis B e Antigens ; Illicium/chemistry* ; Phenyl Ethers