Schizandrin B

J Appl Toxicol. 2014 Dec;34(12):1311-9.

Protective effects of schizandrin and schizandrin B towards cisplatin nephrotoxicity in vitro.[Pubmed: 24155209]

Renal proximal tubular epithelial cells are the main targets of toxic drugs such as cisplatin (CisPt), an alkylating agent indicated for the treatment of solid organ tumors. Current techniques aiming at reducing nephrotoxicity in patients receiving CisPt are still not satisfactory as they can only partially prevent acute kidney injury. New nephroprotective strategies remain to be developed.
METHODS AND RESULTS:
In the present in vitro study, schizandrin (Schi) and Schizandrin B (Schi B), major phytochemicals from Schisandra chinensis (Turcz.) Baill. fruits, were tested on HK-2 cells along four processes that could help alleviate CisPt toxicity. Results indicated that: (i) both Schi and Schi B enhanced cell survival via reducing apoptosis rate; (ii) only Schi showed moderate effects towards modulation of regeneration capacities of healthy cells; (iii) both Schi and Schi B limited extracellular matrix deposition; and (iv) both compounds could help preventing dedifferentiation processes via the β-catenin pathway.
CONCLUSIONS:
Schi and Schi B present promising activities for future development of protective agents against CisPt nephrotoxicity.

Zhongguo Yao Li Xue Bao. 1989 Jul;10(4):353-6.

Action of schizandrin B, an antioxidant, on lipid peroxidation in primary cultured hepatocytes.[Pubmed: 2624122]

METHODS AND RESULTS:
The action of Schizandrin B (Sin B) was observed in freshly isolated hepatocytes damaged by FeSO4/cysteine and CCl4. Two types of free radicals, .OH and .CCl3, generated from FeSO4/cysteine and CCl4, respectively, induced lipid peroxidation in hepatocytes. It was found that the speed of lipid peroxidation (MDA production) and the degree of alteration in hepatocyte morphology were closely related to the type of free radicals. MDA production and membrane protrusion of hepatocytes injuries by FeSO4/cysteine were faster and more severe than those observed with CCl4. Sin B was shown to decrease the production of MDA and the release of GPT and LDH, and to increase hepatocyte viability as well as maintaining the integrity of the hepatocyte membrane surface. These actions of Sin B were stronger than vitamin E at the same concentration. It was observed that no inhibitory effect of phenobarbital, a typical inducer of cytochrome P-450, as Sin B induced liver cytochrome P-450, on MDA production in hepatocytes damaged by FeSO4/cysteine.
CONCLUSIONS:
The results suggest that Sin B possesses antioxidant activity.

J. Pract. Med., 2012, 28(15):2506-9.

Experimental research on Schizandrin B enhancing sensitivity to paclitaxel on rats with mammary carcinoma.[Reference: WebLink]

To investigate the effects of Schizandrin B (Sch B) on enhancing sensitivity to paclitaxel (PTX) on rats with mammary carcinoma.
METHODS AND RESULTS:
Fifty BALB/c rats were randomly divided into five groups, 10 animals of each group: a normal control (NC) group, model control (MC) group, PTX group, Sch B group and PTX + Sch B group. Sch B was administered to the rats by intraperitoneal injection at a dose of 10mg/kg once per day for 22 days. while PTX was every 2 days. The body weight, gross tumor volume, inhibition rate of tumor growth and organ index were observed. Compared with the MC group, the body weight in both the PTX group and Sch B + PTX group began to decrease since the 7th day of administration, the difference in weight was significant by statistics. Compared with the PTX group, the body weight in the Sch B + PTX group was elevated, but the difference was not significant. The inhibition rate in the PTX group was 15.7% and that in the Sch B + PTX group 25.9%. Compared with the MC group, the spleen index in PTX group and the Sch B + PTX group was significantly lower (P = 0.008 and 0.000, respectively). Compared with the PTX group, the spleen index in the Sch B + PTX group was lower, but the difference was not significant. Compared with the PTX group, the thyroid and adrenal gland index in the Sch B + PTX group was significantly elevated (P = 0.000 and 0.011, respectively).
CONCLUSIONS:
Combination of Sch B and PTX can enhance anti-tumor effects and relieve side effects of PTX on rats with mammary carcinoma.

Nan Fang Yi Ke Da Xue Xue Bao. 2012 Apr;32(4):583-5, 592.

[Effect of schizandrin B on H(2)O(2)-induced apoptosis of human hepatocytes in vitro: role of Fas pathway].[Pubmed: 22543149]

To investigate the role of Fas pathway in H(2)O(2)-induced apoptosis of L02 human hepatocytes and the effect of schisandrin B on Fas pathway.
METHODS AND RESULTS:
Real-time quantitative PCR was used to detect the expressions of FAS, fas associated death domain protein (FADD) and caspase-8 mRNA in L02 cells exposed to H(2)O(2). Flow cytometry was employed to assess the cell apoptosis. ELISA, Western blotting and spectrophotometric assay were performed to determine the expressions of FAS protein, FADD protein and caspase-8 activity. Within the dose range of 5-15 mol/L, schisandrin B dose-dependently inhibited FAS and FADD expressions and caspase-8 activation.
CONCLUSIONS:
Schisandrin B can partially inhibit H(2)O(2)-induced L02 cell apoptosis possibly by affecting the FAS-FADD-caspase-8 pathway.

Chinese Pharmacological Bulletin, 2014, 30(4):523-7.

Protective effect of schizandrin B against oxidative damage of UVB irradiated HaCaT cells and its molecular mechanism.[Reference: WebLink]

To investigate the inhibitory effect of Schizandrin B (SchB) on ultraviolet radiation b (UVB) radiation-induced apoptosis of HaCaT cells.
METHODS AND RESULTS:
Methyl thiazolyl tetrazolium (MTT) assay was used to examine the effect of SchB on cell viability recovery. Cell apoptosis and necrosis were measured by Hochest33342 staining. The p53, p21 and Caspase-3 mRNA expressions were examined by RT-PCR. In this study, we found that Sch B attenuated UVB-induced toxicity in HaCaT cells. Through Hoechst 33342 stain, we visualized that SchB could inhibit UVB-induced HaCaT cell death. The result demonstrated that p53, p21 and Caspase-3 mRNA levels decreased compared with the control group.
CONCLUSIONS:
Sch B attenuates the UVB-induced toxicity of HaCaT by inhibiting apoptotic gene expression. It plays a role in antiphotoaging.