Syzygium jambolanum and Cephalandra indica homeopathic preparations inhibit albumin glycation and protect erythrocytes: an in vitro study.

BACKGROUND: Diabetes mellitus is a common endocrine disorder characterized by hyperglycemia eventually resulting in long-term complications. Increased glycation of proteins is implicated in the pathogenesis of complications. For treatment of diabetes, Syzygium jambolanum and Cephalandra indica are frequently prescribed in homeopathy. However their role in glycation is not well elucidated. The present study aimed to evaluate the role of these homeopathic preparations in glycation induced structural modifications and further to examine their cellular protection ability. METHODS: In human erythrocytes, in vitro mother tincture and dilutions of S. jambolanum (Sj ф, 30c, 200c), C. indica (Ci ф, 30c, 200c) and standard antiglycator (AG) were compared and their antiglycation potential assessed by the estimating different markers of glycation (frcutosamines, carbonyls, bound sugar), structural modifications (free amino and thiol group). Phytochemical characterization (total phenolic, flavonoids and glycosides contents) was performed. RESULTS: The homeopathic preparations have different mode of action on albumin glycation modifications. Sj ф preparation demonstrated effective inhibition of all glycation, structural modifications except amino group protection. When dilutions were compared, Sj preparations showed reduction of glycation, structural modifications. All preparations showed significant erythrocyte protection. Sj ф preparation exhibited noteworthy antiglycation and cell protection ability as compared to AG. CONCLUSION: These homeopathic preparations especially Sj ф prevented glycation induced albumin modifications and subsequent toxicity in human eryrthrocytre in vitro. Further investigation of their potential as antiglycators is justified.

Kangfuxin Liquid Ameliorates Dextran Sulfate Sodium (DSS)-Induced Acute Ulcerative Colitis in Mice by Modulating Immune Response and Suppressing Inflammation.

BACKGROUND The aim of this study was to determine the effect of kangfuxin liquid (KFXL) on inflammatory response, and its underlying mechanism in treating acute ulcerative colitis (UC) in mice induced by dextran sulfate sodium (DSS). MATERIAL AND METHODS Mice were provided drinking water containing DSS (3%) for 7 days to induce acute enteritis. The mice were divided into 6 groups: a control group, a DSS-induced (vehicle) group, a sulfasalazine (SASP) group, and low-, medium-, and high-dose kangfuxin liquid groups. Disease activity index (DAI), colon mucosa damage index (CMDI), histopathological score (HS), and organ index were monitored daily. The levels of interleukin-1ß (IL-1ß), interleukin-10 (IL-10) in serum and interleukin-17 (IL-17) and epidermal growth factor (EGF) in colon tissue were assessed by enzyme-linked immunosorbent assay (ELISA). Flow cytometry was used to assess the changes of T lymphocyte subsets in spleens of mice to evaluate the therapeutic effect of drugs on acute UC in mice. RESULTS Different doses of kangfuxin liquid reduced the DAI, CMDI, and HS scores (P<0.01 or P<0.05) of acute UC mice, reduced the level of IL-1ß and IL-17 in serum, increased the expression of IL-10 in serum and EGF in colon tissue, increased the number of CD3⁺ T cells, and decreased the level of CD4⁺ T cells and the ratio of CD4⁺/CD8⁺. CONCLUSIONS Kangfuxin liquid has a therapeutic effect on DSS-induced acute UC in mice, and its mechanism of action may be associated with regulating immune function and reducing intestinal inflammatory response.

[Protective effect of musk extract on rat's cerebral cortical neurons with inflammatory injury].

OBJECTIVE: To investigate the protective effects of musk extract (ME) and its possible mechanism on rat's cerebral cortical neurons with inflammatory injury induced by lipopolysaccharide (LPS). METHODS: Neurons and astrocytes from newborn rat cerebral cortex were cultured in vitro respectively, and the astrocyte conditioned medium (ACM), obtained by treating astrocytes with 10 mg/L LPS and different concentrations of ME for 24 h, was added in the culture fluid of neurons. The survival rate and apoptotic rate of neurons were measured by MTT method and AO/EB stain; and the changes of inflammatory factors in the ACM were determined by ELISA. RESULTS: The survival rate (%) of neurons treated by ACM with ME in concentrations of 18 mg/L, 36 mg/L, 72 mg/L and 144 mg/L was 52.55 +/- 3.52, 55.77 +/- 2.36, 64.89 +/- 3.45 and 73.67 +/- 1.80, respectively, significantly higher than that in the model neurons (43.62 +/- 4. 51, P < 0.05), while the apoptotic rate (%) in them, 68.11 +/- 2.16, 44.27 +/- 3.68, 32.56 +/- 2.14 and 21.89 +/- 2.46, respectively, was significantly lower than that in model neurons (71.33 +/- 3.25, P < 0.05 or P < 0.01). Level of IL-6 was decreasing along with the raising of ME concentration in the ACM, showing a concentration-dependent state. CONCLUSION: ME shows apparent protective effect on neurons against inflammatory injury, especially in a high concentration (144 mg/L), which may be associated with the reduction of IL-6 secreted by astrocytes.

[Intestinal mucosa protection of muscovite n ulcerative colitis in rats].

OBJECTIVE: To examine the efficacy of Muscovite on acetic acid-induced ulcerative colitis in rats, and to research the mechanisms of intestinal mucosal protection. METHOD: Ulcerative colitis was induced in rats by intracolonic injection of 2 mL of 7% acetic acid. Rats were treated with three different doses of the Muscovite and SASP at random by intracolonic injecion, the normal saline was considered as control group. The rats were sacrificed and the colons were excised and opened longitudinally. Under a dissecting microscope, gross findings were observed and scored. MPO activity was assayed by spectrophotometry in colonic mucosa. RESULT: Gross finding showed that multiple ulcer with diameter more than 1 cm, surrounded with erosion, erythematous and edema in the proximal colon in ulcerative coltis. The colon from Muscovite treatment group were histopatholgically normal, with slight erosion, erythematous and edema. The colon in SASP group had small ulceration and severe erosion and edema. The score of gloss change were significant lower in Muscovite groups than that in normal saline group (P < 0.01). There were necrosis and exfoliation of mucosa, multiple cystic dilation of mucosa gland, and large number of and inflammation attenuated in Muscovite groups. There nerutrophils and vessel infiltration in ulcerative colitis. The ulceration disappeared were erosion in mucosa and inflammatory cell infiltrating into submucosa in SASP group. Compared with normal saline group, the pathological scale were significant decreased in Muscovite and SASP groups (P < 0.05). The MPO activity was significant increased in colitis tissue compared with normal group (P < 0.001). After administrating with Muscovite or SASP, the level of MPO were significant decreased (P < 0.01). CONCLUSION: Muscovite has the effect of mucosal protection by attenuating the inflammation of colonic mucosa and decreasing the activity of MPO.

[The protective effects of Fufang Biejiafang on bleomycin-induced pulmonary fibrosis in rats].

OBJECTIVE: To explore the possible effects and mechanism of Fufang Biejiafang on a single intratracheal instillation (IT) of bleomycin-induced lung fibrosis model. METHOD: SD rats were treated with a single IT dose of bleomycin or control saline. Chinese medicine group were poured into the stomach after the first day of operation with high dosage, middle dosage and low dosage. On days 7, 14 and 28 following IT bleomycin or saline, 4 mL blood were taken from the abdominal aorta for arterial blood gas analysis. The left lung was fixed for routine light microscopic examination. Bronchoalveolar lavage fluid (BALF) from the right lung was tested the activity of pulmonary surfactant (PS) by the Whihelmy Film Balance, then the right lung was frozen immediately in liquid nitrogen for determination of hydroxyproline concentration. RESULT: Model rats had obviously changes of body weight and hypoxemia and dysfunction of PS on days 7 and improved on days 14. Compared with three dose groups, the middle dose group some degreely improved and PS function. It ameliorate fibrosis because of inhibition of inflammation. CONCLUSION: (1) PS dysfunction resulted in hypoxemia after bleomycin injured alveolar type II (AT II). Fufang biejiafang-middle dose-group ameliorate hypoxemia by remission AT-II injury. (2) Fufang biejiafang may inhibit exudation inflammation and ameliorate fibrosis.

[Mechanisms of muscovite on gastric mucosal protective effect].

OBJECTIVE: To explore the mechanisms of muscovite gastric mucosal protective effect. METHOD: Rat model of chronic gastritis were used. After gastric mucosal injury was induced, the rats were divided into 6 groups and were treated with different drugs. 2 weeks later, the tissue and blood samples were obtained and measured. RESULT: The general conditions, the observations under macroscopy, microscope and electron microscope of the middle and high dose of muscovite groups resembled those of the normal group. Their PH levels were higher than those of the model group, and the rates of intestinal metaplasia were lower, but the PGE2 level of the middle dose of muscovite group was the highest. CONCLUSION: Muscovite can be adsorbed on the surface of the gastric mucosa. It has gastric mucosal protective effect by improving excretion of mucus and synthesis of PGE2 in gastric mucosa, restraining gastric acid, reversing of intestinal metaplasia and decreasing inflammation cells.

Protective potentials of a potentized homeopathic drug, Lycopodium-30, in ameliorating azo dye induced hepatocarcinogenesis in mice.

The protective potentials of a potentized homeopathic drug, Lycopodium-30, prepared from extract of spores of a plant, Lyocopodium clavatum (Fam: Lycopodiaceae) and used as a remedy for various liver ailments, have been tested in mice chronically fed p-dimethyl amino azo benzene (p-DAB) - an initiator, and phenobarbital (PB) - a promoter of hepatic cancer, by using some cytogenetic endpoints like chromosome aberrations (CA), micronuclei (MN), mitotic index (MI) and sperm head abnormality (SHA), and toxicity biomarkers like acid and alkaline phosphatases (AcP and AlkP, respectively), alanine and aspartate amino transferases (ALT and AST, respectively) and lipid peroxidation (LPO) and reduced glutathione (GSH) activities. The effects of chronic treatment of the carcinogens were assessed at different intervals of fixation, namely, at day 7, 15, 30, 60, 90 and day 120, and compared with that of mice fed conjointly with the carcinogens and the homeopathic remedy. Both the assay systems indicated considerable protective potentials of the homeopathic remedy against p-DAB induced hepatocarcinogenesis in mice.

Inhibitory effect of polypeptides from Chlamys farreri on UVB-induced apoptosis and DNA damage in normal human dermal fibroblasts in vitro.

AIM: To investigate the effect of polypeptide from Chlamys farreri (PCF) on ultraviolet B (UVB)-induced apoptosis and DNA damage in cultured normal human dermal fibroblasts. METHODS: MTT assay was used to measure the viability of cells. Measurements of apoptosis and cytosolic free [Ca2+]i were performed with flow cytometry. The comet assay was employed to detect DNA damage in individual cell. RESULTS: PCF (0.25 %-1%) greatly enhanced the proliferative capacity of cultured fibroblasts irradiated by UVB (1.176 x 10(-4) J/cm2) and markedly reduced apoptosis and the level of DNA damage in a concentration-dependent manner. Meanwhile, PCF could decrease the cytosolic free [Ca2+]i (P<0.01, compared with UVB model). CONCLUSION: The inhibitory effect of PCF on UVB-induced photoaging is due to enhanced abating of UVB-injured DNA and UVB-induced apoptosis. Therefore, PCF can resist UV-induced aging development at the initiation stage.