1 |
Jacoby et al (2001)35
|
Sprague-Dawley derived albino rats |
Daily oral dosing of 5 or 50 mg/kg |
1 × intraperitoneal (IP) dose of cisplatin or doxorubicin on day 3 |
11 days |
Rats receiving MGN-3 were healthier; gained weight and had a lower incidence of diarrhea and gross intestinal pathology compared with control |
2 |
Endo and Kanbayashi (2003)36
|
BALB/c female mice |
0.1 mL at 10 mg/mL in water or by IP daily 1 wk before cisplatin |
Single shot of cisplatin (0.1 mL at the concentration of 15 mg/kg) |
28 days |
MGN-3 (both orally and IP) showed accelerated protection against severe loss of body weight of mice due to cisplatin. The result was statistically significant |
3 |
Badr El-Din et al (2008)37
|
Female Swiss albino mice inoculated with Ehrlich ascites carcinoma (EAC) cells, bearing solid tumors |
MGN-3 dissolved in 0.9% saline given via IP or intratumoral injections at 40 mg/kg body weight (BW) daily for 5 wk |
Nil |
5 wk |
MGN-3 significantly delayed growth in both tumor volume (63.27%) and tumor weight (45.2%) compared with control, through increased apoptosis of EAC cells (1.8-fold), influenced plasma cytokine production, downregulated immune suppressing cytokine IL-10, and increased NK cells activity. No adverse side effects due to MGN-3 treatment were observed |
4 |
Noaman et al (2008)38
|
Female Swiss albino mice inoculated with EAC cells, bearing solid tumors |
MGN-3 dissolved in 0.9% saline given via IP at 25 mg/kg BW, 6 times a week from day 4 or day 11 after inoculation and end at day 25 |
Nil |
25 days |
MGN-3 suppressed the growth of tumors; normalized lipid peroxidation level, augmented glutathione contents, and enhanced antioxidant enzymes activity in blood, liver, and tumor tissue. More pronounced effects were observed when treated by MGN-3 as early as day 4 |
5 |
Pérez-Martínez et al (2015)34
|
NOD-scidIL-2Rgnull mice injected intravenously (IV) with NB-1691luc 2 × 105 neuroblastoma cells |
100 μg/mL overnight for activation of NK cells |
NK cells (fresh or MGN-3 activated). NK cellular IV therapy began 7 days after tumor cells inoculation, twice a week for 4 wk |
4 wk |
MGN-3 stimulated NK cells inhibited neuroblastoma growth and increased survival compared with control. The results were statistically significant |
6 |
Badr El-Din et al (2016)39
|
Male Wistar rats |
1 dose of 40 mg/kg BW via IP injection every other day a total of 8 mo |
Orally administered carcinogenic MNNG (N-methyl-N′-nitro-N-nitrosoguanidine) at 200 mg/kg BW daily for 2 weeks |
8 mo |
MGN-3 significantly lowered incidence of dysplasia and gastric cancer when combined with MNNG; effects observed include suppression of Ki-67 tumor marker, upregulation of apoptotic gastric cancer cells via mitochondrial-dependent pathway, and protection against decrease in lymphocyte levels |
7 |
Badr El-Din et al (2016)40
|
Female Swiss albino mice inoculated with EAC cells, bearing solid tumors |
1 dose of 40 mg/kg BW via IP injection every other day starting from day 8 until day 30 |
Paclitaxel at a dose of 2 mg/kg BW every other day starting from day 8 until day 30 |
30 days |
MGN-3 plus paclitaxel significantly suppressed tumor volume (88%) compared with paclitaxel only (77%) or MGN-3 only (59%). Inhibition of tumor growth was associated with reduced cancer cell proliferation, increased DNA damage and apoptosis |
8 |
Badr El-Din et al (2016)41–Abstract only |
Male albino rats |
25 mg/kg BW 5 times/week IP for 2 wk prior to receiving carcinogens and continued for 20 wk |
Carcinogenic NDEA (N-nitrosodiethylamine) (200 mg/kg BW) single dose IP, plus promoter CCl4 (3 mL/kg BW) weekly subcutaneously for 6 weeks |
20 wk |
MGN-3 inhibited hepatocarcinogenesis induced by NDEA and CCI4 via induction of apoptosis and inhibition of cancer cell proliferation; maintained AST, ALT, ALP, and gamma-GT levels close to normal values |