Objective: Diuresis and removing urinary calculus action of Jieshitong tablet were studied. Methods: Metabolic cage method of rats was adopted to be engaged in diuresis experiment; glycol and ammonium chloride had been given orally for 30 days to form concretion model so that a removing urinary calculus trial could be done. Results: High and low doses of Jeshitong tablet both had significant diuresis effect, total urinary output in 3h of drug group increased about 50% than that of control group. Concretio formative rates of Jeshitong tablet group significantly decresed; the stronger removing urinary calculus action, the higher Jieshitong concentraction was. Conclusion: Jieshitong tablet had diuresis and removing urinary calculus action.

Adenocarcinoma ; pathology ; Adenocarcinoma, Papillary ; pathology ; Aged, 80 and over ; Carcinoma, Renal Cell ; pathology ; Duodenal Neoplasms ; pathology ; Humans ; Kidney Neoplasms ; pathology ; Lung Neoplasms ; pathology ; Male ; Neoplasms, Multiple Primary ; pathology ; Sarcoma ; pathology ; Stomach Neoplasms ; pathology

Adenoma, Villous ; metabolism ; pathology ; surgery ; Aged ; Diagnosis, Differential ; Female ; Humans ; Keratin-20 ; metabolism ; Keratin-7 ; metabolism ; Mullerian Ducts ; pathology ; Papilloma ; pathology ; Vaginal Neoplasms ; metabolism ; pathology ; surgery

The inundation of Cordyceps sinensis counterfeits in the market makes it difficult to identify. In this study, 21 batches of wild C. sinensis from 3 different regions, 30 batches of naturally cultured C. sinensis and 4 kinds of counterfeits extracted by methanol and water were analyzed using NMR technology. 9 characteristic peaks were defined as quantitative criterion after comparison, and NMR fingerprints of C. sinensis were established. According to the result it is highly similar between naturally cultured C. sinensis and wild ones by comparing their NMR fingerprints. However, NMR spectra of four kinds of adulterants showed differences with C. sinensis. The result also showed that NMR fingerprint of C. sinensis are highly characteristic and specific. The NMR characteristic fingerprint of wild C. sinensis was consistent with the naturally cultured C. sinensis, and it indicated that the chemical constituents of wild C. sinensis and naturally cultured C. sinensis are nearly the same.

Despite recent advances in conventional therapeutic approaches for cancer, the efficacy of chemotherapy for cancer is limited due to the drug resistance and toxic side effects during treatment. To overcome drug resistance, higher doses of the toxic chemotherapy drugs are frequently administered, thus leading to even severe adverse side effects, which have limited their clinical application. Cationic liposome as a novel non-viral carrier for co-delivery of gene and chemotherapy drugs in cancer gene therapy has already attracted more and more attention in recent years. Most importantly, this combined strategy can generate a significant synergistic effect, which can silence the related gene expression and increase the concentration of the intracellular chemotherapy drugs. This approach allows the use of a much lower dose of the chemotherapy drugs to achieve same therapeutic effect, which may have the potential for overcoming some major limitations of the conventional chemotherapy. In conclusion, co-delivery of gene and chemotherapy drugs with cationic liposome delivery system will play a vital role in the future and especially could be a promising clinical treatment for drug-resistant tumors.
Animals ; Antineoplastic Combined Chemotherapy Protocols ; administration & dosage ; therapeutic use ; Cations ; Cell Line, Tumor ; DNA ; administration & dosage ; genetics ; Drug Carriers ; Drug Delivery Systems ; Gene Transfer Techniques ; Genetic Therapy ; methods ; Humans ; Liposomes ; administration & dosage ; chemistry ; Neoplasms ; therapy ; RNA, Small Interfering ; administration & dosage ; genetics

AIMTo explore the effects of limb ischemic preconditioning (LIP) on cerebral ischemia/reperfusion injuries.

METHODSThirty six wistar rats, of which bilateral vertebral arteries were occluded permanently, were randomly divided into the following 6 groups: control group, cerebral ischemic group, limb ischemic group, LIP 0 d group (cerebral ischemia was given immediately after LIP), LIP 1 d group (cerebral ischemia was given 1 d after LIP) and LIP 2 d group (cerebral ischemia was given 2 d after LIP). Global cerebral ischemia was performed by four vessels occlusion in rats. LIP was performed by occluding the bilateral femoral arteries for 10 min 3 times in a interval of 10 min. The histological grade and pyramidal neuronal density in the CA1 hippocampus were measured to quantitate the degree of hippocampal injury under thionin staining.

RESULTSThe histological grade was increased and the pyramidal neuronal density was decreased in the CA1 hippocampus of the cerebral ischemic group (P < 0.01). The damage of the CA1 hippocampus in LIP 0 d group was significantly diminished, which represented by decreased histological grade and increased neuronal density compared with the cerebral ischemic group (P < 0.01). But the CA1 hippocampus still showed obvious injuries in the LIP 1 d and LIP 2 d group.

CONCLUSIONLIP performed immediately prior to cerebral ischemia could confer obvious protective effects on CA1 hippocampus against cerebral ischemia/reperfusion injuries. But LIP performed 1 d and 2 d prior to cerebral ischemia could not afford the protection against injuries induced by cerebral ischemia/reperfusion.

Animals ; Brain Ischemia ; prevention & control ; Extremities ; blood supply ; Hippocampus ; blood supply ; Ischemic Preconditioning ; methods ; Rats ; Rats, Wistar ; Reperfusion Injury ; prevention & control

AIMTo explore roles of metabotropic glutamate receptor1/5 (mGluR1/5) in the induction of brain ischemic tolerance (BIT) induced by cerebral ischemic preconditioning (CIP), influences of mGluR1/5 ligand (s)-4-carboxy-3-hydroxy- phenylglycine ((s)-4C3HPG) on the induction of BIT and expression of glial fibrillary acidic protein (GFAP) in the hippocampus were observed.

METHODSThionin staining and GFAP immunohistochemistry staining in rat 4 vessel occlusion (4VO) brain ischemic model was used. Thirty-six rats, of which bilateral vertebral arteries were occluded permanently by electrocautery, were divided into the following 4 groups: sham group; ischemic insult group, BIT group and (s)-4C3HPG group. According to dosages of (s)-4C3HPG used, the (s)-4C3HPG group, was further divided into 0.2 mg, 0.04 mg and 0.008 mg subgroups. All the rats were killed 7 d after the operation or the final ischemic treatment.

RESULTS(1) The ischemic insult for 8 min increased the histological grade (HG), decreased the pyramidal neuronal density (ND) and increased the expression of GFAP significantly (P < 0.05 vs sham) (2) The CIP prevented the above injury changes in the BIT group. (3) The protective effects of the CIP were blocked by (s)-4C3HFG, as manifested by significant increases in HG and decreases in ND in the (s)-4C3HPG group (P < 0.05 vs sham and BIT groups). The changes were proportional with the dosages of (s)-4C3HPG used.

CONCLUSION(s)-4C3HPG could block the induction of BIT induced by CIP, suggested that mGluR1/5 participate in the induction of BIT.

Animals ; Brain Ischemia ; metabolism ; physiopathology ; Electroencephalography ; Glial Fibrillary Acidic Protein ; metabolism ; Glycine ; analogs & derivatives ; pharmacology ; Ischemic Preconditioning ; Male ; Neuroglia ; metabolism ; Rats ; Rats, Sprague-Dawley ; Receptor, Metabotropic Glutamate 5 ; Receptors, Metabotropic Glutamate ; antagonists & inhibitors ; metabolism

AIMTo investigate the effects of the duration of cerebral ischemic preconditioning(CIP) and interval between CIP and the subsequent ischemic insult on the protection of CIP against delayed neuronal death (DND) in the CA1 hippocampus normally induced by brain ischemic insult.

METHODSFour-vessel occlusion cerebral ischemic model of rats (54) was used. The brain of the rats was sectioned and stained with thionin to show DND in the CA1 hippocampus.

RESULTSNo DND was found in the hippocampus of the rats subjected to sham operation and CIP, in which 3 min cerebral ischemic preconditioning was performed. Obvious destruction of the CA1 hippocampus was found in brain ischemic insult group, in which histological (HG) was 2-3 in 6 min and 10 min ischemia subgroups and grade 3 in 15 min ischemia subgroup. In CIP + brain ischemic insult group, no obvious neuronal damage was found in 3 min-3d-6 min (CIP for 3 min was followed by a brain ischemic insult for 6 min at an interval of 3 d, the same as the following) and 3 min-3 d-10 min groups, indicating that CIP effectively protected neurons of the CA1 hippocampus against DND normally induced by ischemic insult for 6 or 10 min. However, in 3 min-1 d-10 min and 3 min-3 d-15 min groups, the protective effect of CIP was lower than that in the 3 min-3 d-10 min group. The quantitative analysis of the protective effect of CIP on the CA1 hippocampal neurons showed that there was no significant difference in protecting number and protecting index between 3 min-3 d-6 min and 3 min-3 d-10 min groups (P > 0.05). However, the growth index in 3 min-3 d-10 min group was obvious larger than that in 3 min-3 d-6 min (P < 0.05).

CONCLUSIONAlthough the protective effects of CIP in 3 min-3 d-6 min and 3 min-3 d-10 min groups were similar, the protective effect of CIP in 3 min-3 d-10 min group was sensitively found. Maximal protective potential of CIP could be induced when using the time parameters of 3 min-3 d-10 min to establish the model of global cerebral ischemic tolerance.

Animals ; Brain Injuries ; pathology ; prevention & control ; Brain Ischemia ; pathology ; prevention & control ; Cell Death ; Hippocampus ; pathology ; Ischemic Preconditioning ; Male ; Neurons ; pathology ; Rats ; Rats, Wistar ; Time Factors

To explore the role of NO in the induction of brain ischemic tolerance (BIT) in vivo, the effect of nitric oxide synthase (NOS) inhibitor L-NAME on the induction of BIT induced by cerebral ischemic preconditioning (CIP) was investigated in the hippocampal CA1 subfield in CIP and ischemic insult models established by rat four-vessel occlusion using brain tissue section and thionine staining methods. Fifty-four male Wistar rats were divided into 6 groups: (1) sham-operated group (n=6): bilateral common arteries were separated without occluding the cerebral blood flow; (2) ischemia group (n=6): an ischemic insult for 10 min was given; (3) CIP+ischemia group (n=6): 3-min CIP was preformed 72 h prior to 10-min ischemic insult; (4) L-NAME group (total n=24, n=6 for each subgroup): L-NAME (5 mg/kg, i.p.) was administered 1 h prior to CIP and 1, 12 and 36 h after CIP, respectively. Other procedures were the same as those for the CIP+ischemia group; (5) L-NAME+L-Arg group (n=6): L-NAME (5 mg/kg, i.p.) and L-Arg (300 mg/kg, i.p.) were administered 1 h prior to CIP, other procedures were the same as those for the L-NAME group; (6) L-NAME+ischemia group (n=6): L-NAME (5 mg/kg, i.p.) was administered 72 h before the 10-min ischemic insult. The results showed that (1)10-min ischemic insult resulted in an increase in the histological grade (indicating a more serious tissue injury) and a decrease in pyramidal neuronal density (P<0.01); (2) the histological grade and neuronal density in hippocampal CA1 in the CIP+ischemia group were similar to those in the sham-operated group (P>0.05); (3) in the L-NAME group, administration of L-NAME brought about an increase in the histological grade and a decrease in neuronal density (P<0.01), suggesting that L-NAME blocked the protection of CIP; (4) the neuronal damage in L-NAME+L-Arg group was slighter than that in the L-NAME group, but still more serious than that in the CIP+ischemia group, suggesting that L-Arg partly reversed the blocking effect of L-NAME; (5) the morphological representations in L-NAME+ischemia group were basically similar to those in the ischemia group. The results mentioned above indicate that NO is involved in the induction of BIT in vivo. The blocking effect of L-NAME administered at 36 h after CIP was obviously weaker than the effects of L-NAME administered 1 h prior to CIP, and 1 or 12 h after CIP. It is suggested that NO is involved in the induction of BIT at an early stage and that the involvement might take place via activating cascades of the events.
Animals ; Brain Ischemia ; physiopathology ; prevention & control ; Enzyme Inhibitors ; pharmacology ; Hippocampus ; physiology ; Ischemic Preconditioning ; methods ; Male ; NG-Nitroarginine Methyl Ester ; pharmacology ; Nitric Oxide ; physiology ; Nitric Oxide Synthase ; antagonists & inhibitors ; Rats ; Rats, Wistar

To explore the role of metabotropic glutamate receptor 2/3 mGluR 2/3 in the induction of brain ischemic tolerance (BIT), the influences of mGluR2/3 antagonist alpha-methyl-(4-tetrazolyl-phenyl) glycine (MTPG) on the induction of BIT and expression of glial fibrillary acidic protein (GFAP) in the hippocampus were observed using thionin staining and GFAP immunohistochemical staining in a rat brain ischemic model with four-vessel occlusion (4VO). Fifty-four rats, of which bilateral vertebral arteries were occluded permanently by electrocautery, were divided into 5 groups: (1) sham operated group (n=8): the bilateral carotid common arteries (BCCA) were separated, but the blood flow was not blocked; (2) ischemia group (n=8): the blood flow of BCCA was blocked for 8 min; (3) ischemic preconditioning (IP) group (n=8): the blood flow of BCCA was occluded for 3 min as a cerebral ischemic preconditioning (CIP), and then the rats were exposed to an 8-min brain ischemic insult 24 h after the CIP; (4) MTPG+IP group (n=22): MTPG was administered 20 min before the CIP, then the rats were exposed to an 8-min brain ischemia insult 24 h after the CIP. In order to examine dosage dependency in the effect of MTPG, 4 dosages of MTPG (0.4, 0.2, 0.04 and 0.008 mg) were administered; (5) MTPG+ischemia group (n=8): an ischemic insult for 8 min was given 24 h after the administration of MTPG (0.2 mg). MTPG was injected into the right lateral cerebral ventricle. The results obtained are as follows. (1) Ischemic insult for 8 min increased the histological grade (HG) and reduced the neuronal density (ND) significantly, and also increased the expression of GFAP significantly (P<0.05 vs sham-operated group). (2) In the IP group, the above changes were not observed, indicating that CIP could protect pyramidal neurons against the ischemic insult. (3) The protective effects of CIP were blocked by MTPG, as manifested by the significant increase in HG and decrease in ND in the MTPG+IP group (P<0.05 vs sham-operated group). The changes were dose-dependent. (4) No obvious difference in the HG, ND and expression of GFAP was detected between the groups of MTPG+ischemia and ischemia. The above results indicate that MTPG blocks the induction of BIT induced by CIP, suggesting that mGluR2/3 participates in the induction of BIT.
Alanine ; analogs & derivatives ; pharmacology ; Animals ; Brain Ischemia ; physiopathology ; Hippocampus ; blood supply ; drug effects ; physiopathology ; Ischemic Preconditioning ; methods ; Male ; Rats ; Rats, Sprague-Dawley ; Receptors, Metabotropic Glutamate ; antagonists & inhibitors ; Reperfusion Injury ; physiopathology ; prevention & control ; Tetrazoles ; pharmacology